Leukemia associated with HYPERPLASIA of the lymphoid tissues and increased numbers of circulating malignant LYMPHOCYTES and lymphoblasts.
A progressive, malignant disease of the blood-forming organs, characterized by distorted proliferation and development of leukocytes and their precursors in the blood and bone marrow. Leukemias were originally termed acute or chronic based on life expectancy but now are classified according to cellular maturity. Acute leukemias consist of predominately immature cells; chronic leukemias are composed of more mature cells. (From The Merck Manual, 2006)
A neoplasm characterized by abnormalities of the lymphoid cell precursors leading to excessive lymphoblasts in the marrow and other organs. It is the most common cancer in children and accounts for the vast majority of all childhood leukemias.
Clonal expansion of myeloid blasts in bone marrow, blood, and other tissue. Myeloid leukemias develop from changes in cells that normally produce NEUTROPHILS; BASOPHILS; EOSINOPHILS; and MONOCYTES.
Circumscribed masses of foreign or metabolically inactive materials, within the CELL NUCLEUS. Some are VIRAL INCLUSION BODIES.
A chronic leukemia characterized by abnormal B-lymphocytes and often generalized lymphadenopathy. In patients presenting predominately with blood and bone marrow involvement it is called chronic lymphocytic leukemia (CLL); in those predominately with enlarged lymph nodes it is called small lymphocytic lymphoma. These terms represent spectrums of the same disease.
A malignant disease of the B-LYMPHOCYTES in the bone marrow and/or blood.
Proteins that are normally involved in holding cellular growth in check. Deficiencies or abnormalities in these proteins may lead to unregulated cell growth and tumor development.
Leukemia induced experimentally in animals by exposure to leukemogenic agents, such as VIRUSES; RADIATION; or by TRANSPLANTATION of leukemic tissues.
Proteins found in the nucleus of a cell. Do not confuse with NUCLEOPROTEINS which are proteins conjugated with nucleic acids, that are not necessarily present in the nucleus.
Myeloid-lymphoid leukemia protein is a transcription factor that maintains high levels of HOMEOTIC GENE expression during development. The GENE for myeloid-lymphoid leukemia protein is commonly disrupted in LEUKEMIA and combines with over 40 partner genes to form FUSION ONCOGENE PROTEINS.
Structures that are part of or contained in the CELL NUCLEUS.
Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.
Form of leukemia characterized by an uncontrolled proliferation of the myeloid lineage and their precursors (MYELOID PROGENITOR CELLS) in the bone marrow and other sites.
Proteins whose abnormal expression (gain or loss) are associated with the development, growth, or progression of NEOPLASMS. Some neoplasm proteins are tumor antigens (ANTIGENS, NEOPLASM), i.e. they induce an immune reaction to their tumor. Many neoplasm proteins have been characterized and are used as tumor markers (BIOMARKERS, TUMOR) when they are detectable in cells and body fluids as monitors for the presence or growth of tumors. Abnormal expression of ONCOGENE PROTEINS is involved in neoplastic transformation, whereas the loss of expression of TUMOR SUPPRESSOR PROTEINS is involved with the loss of growth control and progression of the neoplasm.
An advanced phase of chronic myelogenous leukemia, characterized by a rapid increase in the proportion of immature white blood cells (blasts) in the blood and bone marrow to greater than 30%.
Disease having a short and relatively severe course.
The soft tissue filling the cavities of bones. Bone marrow exists in two types, yellow and red. Yellow marrow is found in the large cavities of large bones and consists mostly of fat cells and a few primitive blood cells. Red marrow is a hematopoietic tissue and is the site of production of erythrocytes and granular leukocytes. Bone marrow is made up of a framework of connective tissue containing branching fibers with the frame being filled with marrow cells.
Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.
Therapeutic act or process that initiates a response to a complete or partial remission level.
A 1.5-kDa small ubiquitin-related modifier protein that can covalently bind via an isopeptide link to a number of cellular proteins. It may play a role in intracellular protein transport and a number of other cellular processes.
An acute myeloid leukemia in which abnormal PROMYELOCYTES predominate. It is frequently associated with DISSEMINATED INTRAVASCULAR COAGULATION.
Binary compounds of oxygen containing the anion O(2-). The anion combines with metals to form alkaline oxides and non-metals to form acidic oxides.
Inorganic or organic compounds that contain arsenic.
White blood cells formed in the body's lymphoid tissue. The nucleus is round or ovoid with coarse, irregularly clumped chromatin while the cytoplasm is typically pale blue with azurophilic (if any) granules. Most lymphocytes can be classified as either T or B (with subpopulations of each), or NATURAL KILLER CELLS.
Clonal hematopoetic disorder caused by an acquired genetic defect in PLURIPOTENT STEM CELLS. It starts in MYELOID CELLS of the bone marrow, invades the blood and then other organs. The condition progresses from a stable, more indolent, chronic phase (LEUKEMIA, MYELOID, CHRONIC PHASE) lasting up to 7 years, to an advanced phase composed of an accelerated phase (LEUKEMIA, MYELOID, ACCELERATED PHASE) and BLAST CRISIS.
Within a eukaryotic cell, a membrane-limited body which contains chromosomes and one or more nucleoli (CELL NUCLEOLUS). The nuclear membrane consists of a double unit-type membrane which is perforated by a number of pores; the outermost membrane is continuous with the ENDOPLASMIC RETICULUM. A cell may contain more than one nucleus. (From Singleton & Sainsbury, Dictionary of Microbiology and Molecular Biology, 2d ed)
In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships.
Species of GAMMARETROVIRUS, containing many well-defined strains, producing leukemia in mice. Disease is commonly induced by injecting filtrates of propagable tumors into newborn mice.
Established cell cultures that have the potential to propagate indefinitely.
A malignant disease of the T-LYMPHOCYTES in the bone marrow, thymus, and/or blood.
An acute myeloid leukemia in which 80% or more of the leukemic cells are of monocytic lineage including monoblasts, promonocytes, and MONOCYTES.
The first continuously cultured human malignant CELL LINE, derived from the cervical carcinoma of Henrietta Lacks. These cells are used for VIRUS CULTIVATION and antitumor drug screening assays.
A strain of Murine leukemia virus (LEUKEMIA VIRUS, MURINE) arising during the propagation of S37 mouse sarcoma, and causing lymphoid leukemia in mice. It also infects rats and newborn hamsters. It is apparently transmitted to embryos in utero and to newborns through mother's milk.
Immunologically detectable substances found in the CELL NUCLEUS.
Motifs in DNA- and RNA-binding proteins whose amino acids are folded into a single structural unit around a zinc atom. In the classic zinc finger, one zinc atom is bound to two cysteines and two histidines. In between the cysteines and histidines are 12 residues which form a DNA binding fingertip. By variations in the composition of the sequences in the fingertip and the number and spacing of tandem repeats of the motif, zinc fingers can form a large number of different sequence specific binding sites.
Proteins which bind to DNA. The family includes proteins which bind to both double- and single-stranded DNA and also includes specific DNA binding proteins in serum which can be used as markers for malignant diseases.
A neoplastic disease of the lymphoreticular cells which is considered to be a rare type of chronic leukemia; it is characterized by an insidious onset, splenomegaly, anemia, granulocytopenia, thrombocytopenia, little or no lymphadenopathy, and the presence of "hairy" or "flagellated" cells in the blood and bone marrow.
The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.
Leukemia L1210 is a designation for a specific murine (mouse) leukemia cell line that was originally isolated from a female mouse with an induced acute myeloid leukemia, which is widely used as a model in cancer research, particularly for in vivo studies of drug efficacy and resistance.
The level of protein structure in which combinations of secondary protein structures (alpha helices, beta sheets, loop regions, and motifs) pack together to form folded shapes called domains. Disulfide bridges between cysteines in two different parts of the polypeptide chain along with other interactions between the chains play a role in the formation and stabilization of tertiary structure. Small proteins usually consist of only one domain but larger proteins may contain a number of domains connected by segments of polypeptide chain which lack regular secondary structure.
Processes that stimulate the GENETIC TRANSCRIPTION of a gene or set of genes.
Microscopy of specimens stained with fluorescent dye (usually fluorescein isothiocyanate) or of naturally fluorescent materials, which emit light when exposed to ultraviolet or blue light. Immunofluorescence microscopy utilizes antibodies that are labeled with fluorescent dye.
The type species of DELTARETROVIRUS that causes a form of bovine lymphosarcoma (ENZOOTIC BOVINE LEUKOSIS) or persistent lymphocytosis.
A species of GAMMARETROVIRUS causing leukemia, lymphosarcoma, immune deficiency, or other degenerative diseases in cats. Several cellular oncogenes confer on FeLV the ability to induce sarcomas (see also SARCOMA VIRUSES, FELINE).
A cell line derived from cultured tumor cells.
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.
The GENETIC TRANSLATION products of the fusion between an ONCOGENE and another gene. The latter may be of viral or cellular origin.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in leukemia.
The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.
Leukemia produced by exposure to IONIZING RADIATION or NON-IONIZING RADIATION.
Recombinant proteins produced by the GENETIC TRANSLATION of fused genes formed by the combination of NUCLEIC ACID REGULATORY SEQUENCES of one or more genes with the protein coding sequences of one or more genes.
Transport proteins that carry specific substances in the blood or across cell membranes.
The process of intracellular viral multiplication, consisting of the synthesis of PROTEINS; NUCLEIC ACIDS; and sometimes LIPIDS, and their assembly into a new infectious particle.
Nuclear phosphoprotein encoded by the p53 gene (GENES, P53) whose normal function is to control CELL PROLIFERATION and APOPTOSIS. A mutant or absent p53 protein has been found in LEUKEMIA; OSTEOSARCOMA; LUNG CANCER; and COLORECTAL CANCER.
Different forms of a protein that may be produced from different GENES, or from the same gene by ALTERNATIVE SPLICING.
Proteins that are coded by immediate-early genes, in the absence of de novo protein synthesis. The term was originally used exclusively for viral regulatory proteins that were synthesized just after viral integration into the host cell. It is also used to describe cellular proteins which are synthesized immediately after the resting cell is stimulated by extracellular signals.
Small double-stranded, non-protein coding RNAs (21-31 nucleotides) involved in GENE SILENCING functions, especially RNA INTERFERENCE (RNAi). Endogenously, siRNAs are generated from dsRNAs (RNA, DOUBLE-STRANDED) by the same ribonuclease, Dicer, that generates miRNAs (MICRORNAS). The perfect match of the siRNAs' antisense strand to their target RNAs mediates RNAi by siRNA-guided RNA cleavage. siRNAs fall into different classes including trans-acting siRNA (tasiRNA), repeat-associated RNA (rasiRNA), small-scan RNA (scnRNA), and Piwi protein-interacting RNA (piRNA) and have different specific gene silencing functions.
CELL LINES derived from the CV-1 cell line by transformation with a replication origin defective mutant of SV40 VIRUS, which codes for wild type large T antigen (ANTIGENS, POLYOMAVIRUS TRANSFORMING). They are used for transfection and cloning. (The CV-1 cell line was derived from the kidney of an adult male African green monkey (CERCOPITHECUS AETHIOPS).)
A gene silencing phenomenon whereby specific dsRNAs (RNA, DOUBLE-STRANDED) trigger the degradation of homologous mRNA (RNA, MESSENGER). The specific dsRNAs are processed into SMALL INTERFERING RNA (siRNA) which serves as a guide for cleavage of the homologous mRNA in the RNA-INDUCED SILENCING COMPLEX. DNA METHYLATION may also be triggered during this process.
A broad category of carrier proteins that play a role in SIGNAL TRANSDUCTION. They generally contain several modular domains, each of which having its own binding activity, and act by forming complexes with other intracellular-signaling molecules. Signal-transducing adaptor proteins lack enzyme activity, however their activity can be modulated by other signal-transducing enzymes
An experimental lymphocytic leukemia originally induced in DBA/2 mice by painting with methylcholanthrene.
An acute leukemia exhibiting cell features characteristic of both the myeloid and lymphoid lineages and probably arising from MULTIPOTENT STEM CELLS.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
Proteins and peptides that are involved in SIGNAL TRANSDUCTION within the cell. Included here are peptides and proteins that regulate the activity of TRANSCRIPTION FACTORS and cellular processes in response to signals from CELL SURFACE RECEPTORS. Intracellular signaling peptide and proteins may be part of an enzymatic signaling cascade or act through binding to and modifying the action of other signaling factors.
Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.
A strain of Murine leukemia virus (LEUKEMIA VIRUS, MURINE) producing leukemia of the reticulum-cell type with massive infiltration of liver, spleen, and bone marrow. It infects DBA/2 and Swiss mice.
Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.
Proteins which maintain the transcriptional quiescence of specific GENES or OPERONS. Classical repressor proteins are DNA-binding proteins that are normally bound to the OPERATOR REGION of an operon, or the ENHANCER SEQUENCES of a gene until a signal occurs that causes their release.
Proteins found in any species of virus.
A promyelocytic cell line derived from a patient with ACUTE PROMYELOCYTIC LEUKEMIA. HL-60 cells lack specific markers for LYMPHOID CELLS but express surface receptors for FC FRAGMENTS and COMPLEMENT SYSTEM PROTEINS. They also exhibit phagocytic activity and responsiveness to chemotactic stimuli. (From Hay et al., American Type Culture Collection, 7th ed, pp127-8)
The process of moving proteins from one cellular compartment (including extracellular) to another by various sorting and transport mechanisms such as gated transport, protein translocation, and vesicular transport.
Aggressive T-Cell malignancy with adult onset, caused by HUMAN T-LYMPHOTROPIC VIRUS 1. It is endemic in Japan, the Caribbean basin, Southeastern United States, Hawaii, and parts of Central and South America and sub-Saharan Africa.
A pyrimidine nucleoside analog that is used mainly in the treatment of leukemia, especially acute non-lymphoblastic leukemia. Cytarabine is an antimetabolite antineoplastic agent that inhibits the synthesis of DNA. Its actions are specific for the S phase of the cell cycle. It also has antiviral and immunosuppressant properties. (From Martindale, The Extra Pharmacopoeia, 30th ed, p472)
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
An acute myeloid leukemia in which 20-30% of the bone marrow or peripheral blood cells are of megakaryocyte lineage. MYELOFIBROSIS or increased bone marrow RETICULIN is common.
A strain of Murine leukemia virus (LEUKEMIA VIRUS, MURINE) isolated from spontaneous leukemia in AKR strain mice.
Translation products of a fusion gene derived from CHROMOSOMAL TRANSLOCATION of C-ABL GENES to the genetic locus of the breakpoint cluster region gene on chromosome 22. Several different variants of the bcr-abl fusion proteins occur depending upon the precise location of the chromosomal breakpoint. These variants can be associated with distinct subtypes of leukemias such as PRECURSOR CELL LYMPHOBLASTIC LEUKEMIA-LYMPHOMA; LEUKEMIA, MYELOGENOUS, CHRONIC, BCR-ABL POSITIVE; and NEUTROPHILIC LEUKEMIA, CHRONIC.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
The initial phase of chronic myeloid leukemia consisting of an relatively indolent period lasting from 4 to 7 years. Patients range from asymptomatic to those exhibiting ANEMIA; SPLENOMEGALY; and increased cell turnover. There are 5% or fewer blast cells in the blood and bone marrow in this phase.
A leukemia/lymphoma found predominately in children and adolescents and characterized by a high number of lymphoblasts and solid tumor lesions. Frequent sites involve LYMPH NODES, skin, and bones. It most commonly presents as leukemia.
Substances that inhibit or prevent the proliferation of NEOPLASMS.
A very toxic anthracycline aminoglycoside antineoplastic isolated from Streptomyces peucetius and others, used in treatment of LEUKEMIA and other NEOPLASMS.
A rare, aggressive variant of MULTIPLE MYELOMA characterized by the circulation of excessive PLASMA CELLS in the peripheral blood. It can be a primary manifestation of multiple myeloma or develop as a terminal complication during the disease.
The phase of chronic myeloid leukemia following the chronic phase (LEUKEMIA, MYELOID, CHRONIC-PHASE), where there are increased systemic symptoms, worsening cytopenias, and refractory LEUKOCYTOSIS.
Mapping of the KARYOTYPE of a cell.
An ERYTHROLEUKEMIA cell line derived from a CHRONIC MYELOID LEUKEMIA patient in BLAST CRISIS.
A lymphoid leukemia characterized by a profound LYMPHOCYTOSIS with or without LYMPHADENOPATHY, hepatosplenomegaly, frequently rapid progression, and short survival. It was formerly called T-cell chronic lymphocytic leukemia.
A strain of PRIMATE T-LYMPHOTROPIC VIRUS 1 isolated from mature T4 cells in patients with T-lymphoproliferation malignancies. It causes adult T-cell leukemia (LEUKEMIA-LYMPHOMA, T-CELL, ACUTE, HTLV-I-ASSOCIATED), T-cell lymphoma (LYMPHOMA, T-CELL), and is involved in mycosis fungoides, SEZARY SYNDROME and tropical spastic paraparesis (PARAPARESIS, TROPICAL SPASTIC).
A chronic leukemia characterized by a large number of circulating prolymphocytes. It can arise spontaneously or as a consequence of transformation of CHRONIC LYMPHOCYTIC LEUKEMIA.
A transcription factor that dimerizes with the cofactor CORE BINDING FACTOR BETA SUBUNIT to form core binding factor. It contains a highly conserved DNA-binding domain known as the runt domain. Runx1 is frequently mutated in human LEUKEMIAS.
A leukemia affecting young children characterized by SPLENOMEGALY, enlarged lymph nodes, rashes, and hemorrhages. Traditionally classed as a myeloproliferative disease, it is now considered a mixed myeloproliferative-mylelodysplastic disorder.
A leukemia/lymphoma found predominately in children and young adults and characterized LYMPHADENOPATHY and THYMUS GLAND involvement. It most frequently presents as a lymphoma, but a leukemic progression in the bone marrow is common.
A rare acute myeloid leukemia in which the primary differentiation is to BASOPHILS. It is characterized by an extreme increase of immature basophilic granulated cells in the bone marrow and blood. Mature basophils are usually sparse.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
A pathologic change in leukemia in which leukemic cells permeate various organs at any stage of the disease. All types of leukemia show various degrees of infiltration, depending upon the type of leukemia. The degree of infiltration may vary from site to site. The liver and spleen are common sites of infiltration, the greatest appearing in myelocytic leukemia, but infiltration is seen also in the granulocytic and lymphocytic types. The kidney is also a common site and of the gastrointestinal system, the stomach and ileum are commonly involved. In lymphocytic leukemia the skin is often infiltrated. The central nervous system too is a common site.
A hydrolase enzyme that converts L-asparagine and water to L-aspartate and NH3. EC 3.5.1.1.
A receptor tyrosine kinase that is involved in HEMATOPOIESIS. It is closely related to FMS PROTO-ONCOGENE PROTEIN and is commonly mutated in acute MYELOID LEUKEMIA.
An aberrant form of human CHROMOSOME 22 characterized by translocation of the distal end of chromosome 9 from 9q34, to the long arm of chromosome 22 at 22q11. It is present in the bone marrow cells of 80 to 90 per cent of patients with chronic myelocytic leukemia (LEUKEMIA, MYELOGENOUS, CHRONIC, BCR-ABL POSITIVE).
A general term for various neoplastic diseases of the lymphoid tissue.
A myelodysplastic/myeloproliferative disorder characterized by myelodysplasia associated with bone marrow and peripheral blood patterns similar to CHRONIC MYELOID LEUKEMIA, but cytogenetically lacking a PHILADELPHIA CHROMOSOME or bcr/abl fusion gene (GENES, ABL).

Establishment of an inducible expression system of chimeric MLL-LTG9 protein and inhibition of Hox a7, Hox b7 and Hox c9 expression by MLL-LTG9 in 32Dcl3 cells. (1/654)

The MLL (HRX/ALL-1 gene is frequently disrupted in infantile leukemias and therapy-related leukemias and fused to various translocation partner genes. We previously showed that chimeric MLL proteins localize in the nuclei in a fashion similar to that of MLL protein even if the partner gene encodes a cytoplasmic protein and indicated the importance of the N-terminal portion of MLL common to various MLL translocations. This time we established an inducible expression system for chimeric MLL-LTG9 and truncated N-terminal MLL proteins (MLL-Zf(-)) in 32Dcl3 cells. By utilizing this system, we were able to show inhibition of Hox a7, Hox b7 and Hox c9 genes' expression by induced MLL-LTG9 and MLL-Zf(-). Up-regulation of Hox a7, Hox b7 and Hox c9 was observed when 32Dcl3 cells were cultured with granulocyte colony stimulating factor (G-CSF) in place of interleukin 3 and induction of MLL-LTG9 and MLL-Zf(-) was shown to suppress this upregulation. At the same time, expression of two mammalian Polycomb group genes, M33 and mel-18, which both reportedly affect Hox genes' expression, was not inhibited by MLL-LTG9 and MLL-Zf(-) induction. These results indicate that MLL has an important effect on the expression of at least some Hox genes in hematopoietic cells and suggest that inhibition of the proper expression of Hox genes by chimeric MLL proteins may dysregulate hematopoietic cell differentiation and proliferation, which then can lead to leukemogenesis.  (+info)

Expression of Drosophila trithorax-group homologues in chick embryos. (2/654)

Mll, Brg1 and Brm are vertebrate homologues of Drosophila trithorax group (trxG) genes. We isolated chicken Mll cDNA clones, and examined patterns of Mll, Brg1 and Brm expression in chick embryos. All three genes were expressed from embryonic stage 2 onwards. Mll transcripts were just detectable in all tissues by in situ hybridization, with highest level in dorsal neural tube and notochord. Brg1 transcripts were readily detectable in all tissues, with highest levels in dorsal neural tube, dorsal trunk epithelium and limb bud epithelium and mesenchyme. Brm transcripts were more restricted, being found in dermomyotome, notochord, dorsal limb bud epithelium, eye and the roof and floor plates of the neural tube.  (+info)

Transcriptional inhibition of p53 by the MLL/MEN chimeric protein found in myeloid leukemia. (3/654)

The t(11;19)(q23;p13.1) translocation is frequently found in adult myeloid leukemia. In the MLL/MEN fusion protein generated by this translocation, most of the coding region of the MEN protein, an RNA polymerase II elongation factor, is fused to the N-terminal third of the MLL protein, a possible transcriptional regulator. However, the molecular mechanism of leukemogenesis by the fusion protein remains unclear. We investigated the effects of the fusion protein on p53 function using luciferase assays. Overexpression of the fusion protein suppressed the transactivation ability of p53. This negative effect of the fusion protein on p53 function was dependent on the region derived from MEN. Moreover, p53 coimmunoprecipitated with MLL/MEN as well as MEN, suggesting that the fusion protein binds to p53 through the MEN region. We found that MEN binding to p53 was mediated by its N-terminal region and repression of p53 transcriptional activity was mediated by its C-terminal region. We also found that these two functional regions were essential for the transformation of Rat1 cells mediated by MEN. Although we could not demonstrate a functional difference between MLL/MEN and MEN in this study, these data suggest that the MLL/MEN chimeric transcriptional regulator may exert its oncogenic activity by inhibiting the function of the p53 tumor-suppressor protein by binding to it. Our findings provide a novel insight into the leukemogenic mechanism exerted by the t(11;19)(q23;p13.1) translocation.  (+info)

MSF (MLL septin-like fusion), a fusion partner gene of MLL, in a therapy-related acute myeloid leukemia with a t(11;17)(q23;q25). (4/654)

MLL (ALL1, Htrx, HRX), which is located on chromosome band 11q23, frequently is rearranged in patients with therapy-related acute myeloid leukemia who previously were treated with DNA topoisomerase II inhibitors. In this study, we have identified a fusion partner of MLL in a 10-year-old female who developed therapy-related acute myeloid leukemia 17 months after treatment for Hodgkin's disease. Leukemia cells of this patient had a t(11;17)(q23;q25), which involved MLL as demonstrated by Southern blot analysis. The partner gene was cloned from cDNA of the leukemia cells by use of a combination of adapter reverse transcriptase-PCR, rapid amplification of 5' cDNA ends, and BLAST database analysis to identify expressed sequence tags. The full-length cDNA of 2.8 kb was found to be an additional member of the septin family, therefore it was named MSF (MLL septin-like fusion). Members of the septin family conserve the GTP binding domain, localize in the cytoplasm, and interact with cytoskeletal filaments. A major 4-kb transcript of MSF was expressed ubiquitously; a 1.7-kb transcript was found in most tissues. An additional 3-kb transcript was found only in hematopoietic tissues. By amplification with MLL exon 5 forward primer and reverse primers in MSF, the appropriately sized products were obtained. MSF is highly homologous to hCDCrel-1, which is a partner gene of MLL in leukemias with a t(11;22)(q23;q11.2). Further analysis of MSF may help to delineate the function of MLL partner genes in leukemia, particularly in therapy-related leukemia.  (+info)

Physical interaction and functional antagonism between the RNA polymerase II elongation factor ELL and p53. (5/654)

ELL was originally identified as a gene that undergoes translocation with the trithorax-like MLL gene in acute myeloid leukemia. Recent studies have shown that the gene product, ELL, functions as an RNA polymerase II elongation factor that increases the rate of transcription by RNA polymerase II by suppressing transient pausing. Using yeast two-hybrid screening with ELL as bait, we isolated the p53 tumor suppressor protein as a specific interactor of ELL. The interaction involves respectively the transcription elongation activation domain of ELL and the C-terminal tail of p53. Through this interaction, ELL inhibits both sequence-specific transactivation and sequence-independent transrepression by p53. Thus, ELL acts as a negative regulator of p53 in transcription. Conversely, p53 inhibits the transcription elongation activity of ELL, suggesting that p53 is capable of regulating general transcription by RNA polymerase II through controlling the ELL activity. Elevated levels of ELL in cells resulted in the inhibition of p53-dependent induction of endogenous p21 and substantially protected cells from p53-mediated apoptosis that is induced by genotoxic stress. Our observations indicate the existence of a mutually inhibitory interaction between p53 and a general transcription elongation factor ELL and raise the possibility that an aberrant interaction between p53 and ELL may play a role in the genesis of leukemias carrying MLL-ELL gene translocations.  (+info)

Loss of heterozygosity and microsatellite instability at the MLL locus are common in childhood acute leukemia, but not in infant acute leukemia. (6/654)

Rearrangements involving the MLL gene at chromosome 11q23 are associated with leukemia and are present in up to 70% of infant leukemias. Loss of heterozygosity (LOH) has been shown for anonymous polymorphic markers at 11q23 in adult leukemias. To study LOH at the MLL locus, we have identified two new polymorphic microsatellite markers: a GAA repeat (mllGAAn) in intron 6 of the MLL gene and a GA (mllGAn) repeat in the 5' flanking region of the gene, approximately 2 kb upstream of the translation initiation codon. The heterozygosity index of mllGAAn is 0.54, which renders it useful for analyzing LOH. We screened two groups of leukemia patients to study LOH at the mllGAAn marker. Group A (n = 18) was selected on the basis of presentation before 18 months. Cytogenetic and reverse transcription-polymerase chain reaction analysis showed that 9 of these 18 children had translocations involving MLL. No LOH was observed. Group B (n = 36) were randomly selected children who had presented with leukemia between 1993 and 1994. Cytogenetic analysis of this group showed a variety of different chromosomal abnormalities. LOH was shown in 9 of 20 individuals (45%) who were informative. Microsatellite instability (MSI) was demonstrated in 1 of 18 individuals in group A and 5 of 36 individuals (13.9%) in group B. MSI and LOH were observed simultaneously in three individuals. Loss of an allele was confirmed in one individual by fluorescence in situ hybridization. Individuals with MSI or LOH at mllGAAn were selected for analysis at anonymous polymorphic markers D11S1364 and D11S1356, which flank the MLL gene. No LOH or MSI was observed at these markers in those individuals who were informative. These results show that LOH at the MLL gene locus is a common event during leukemogenesis. Furthermore, the presence of MSI at this locus suggests that the region is a hotspot for genetic instability.  (+info)

The mll-AF9 gene fusion in mice controls myeloproliferation and specifies acute myeloid leukaemogenesis. (7/654)

The MLL gene from human chromosome 11q23 is involved in >30 different chromosomal translocations resulting in a plethora of different MLL fusion proteins. Each of these tends to associate with a specific leukaemia type, for example, MLL-AF9 is found mainly in acute myeloid leukaemia. We have studied the role of the Mll-AF9 gene fusion made in mouse embryonic stem cells by an homologous recombination knock-in. Acute leukaemias developed in heterozygous mice carrying this fusion as well as in chimeric mice. As with human chromosomal translocation t(9;11), the majority of cases were acute myeloid leukaemias (AMLs) involving immature myeloblasts, but a minority were acute lymphoblastic leukaemia. The AMLs were preceded by effects on haematopoietic differentiation involving a myeloproliferation resulting in accumulation of Mac-1/Gr-1 double-positive mature myeloid cells in bone marrow as early as 6 days after birth. Therefore, non-malignant expansion of myeloid precursors is the first stage of Mll-AF9-mediated leukaemia followed by accumulation of malignant cells in bone marrow and other tissues. Thus, the late onset of overt tumours suggests that secondary tumorigenic mutations are necessary for malignancy associated with MLL-AF9 gene fusion and that myeloproliferation provides the pool of cells in which such events can occur.  (+info)

Rapid isolation of chromosomal breakpoints from patients with t(4;11) acute lymphoblastic leukemia: implications for basic and clinical research. (8/654)

Chromosomal translocations t(4;11)(q21;q23) are associated with a group of acute lymphoblastic leukemias with very poor prognosis. From the complete sequences of the breakpoint cluster regions of the human MLL and AF-4 translocation partner genes, a novel set of 66 oligonucleotides that facilitates the rapid identification of translocation breakpoints by PCR analysis of genomic DNA was designed. For each breakpoint, a pair of optimally snited primers can be assigned, which improves the monitoring of the disease during treatment. Comparison of the breakpoints with the corresponding parental sequences also contributes to our better understanding of the illegitimate recombination events leading to these translocations.  (+info)

Leukemia, lymphoid is a type of cancer that affects the lymphoid cells, which are a vital part of the body's immune system. It is characterized by the uncontrolled production of abnormal white blood cells (leukocytes or WBCs) in the bone marrow, specifically the lymphocytes. These abnormal lymphocytes accumulate and interfere with the production of normal blood cells, leading to a decrease in red blood cells (anemia), platelets (thrombocytopenia), and healthy white blood cells (leukopenia).

There are two main types of lymphoid leukemia: acute lymphoblastic leukemia (ALL) and chronic lymphocytic leukemia (CLL). Acute lymphoblastic leukemia progresses rapidly, while chronic lymphocytic leukemia has a slower onset and progression.

Symptoms of lymphoid leukemia may include fatigue, frequent infections, easy bruising or bleeding, weight loss, swollen lymph nodes, and bone pain. Treatment options depend on the type, stage, and individual patient factors but often involve chemotherapy, radiation therapy, targeted therapy, immunotherapy, or stem cell transplantation.

Leukemia is a type of cancer that originates from the bone marrow - the soft, inner part of certain bones where new blood cells are made. It is characterized by an abnormal production of white blood cells, known as leukocytes or blasts. These abnormal cells accumulate in the bone marrow and interfere with the production of normal blood cells, leading to a decrease in red blood cells (anemia), platelets (thrombocytopenia), and healthy white blood cells (leukopenia).

There are several types of leukemia, classified based on the specific type of white blood cell affected and the speed at which the disease progresses:

1. Acute Leukemias - These types of leukemia progress rapidly, with symptoms developing over a few weeks or months. They involve the rapid growth and accumulation of immature, nonfunctional white blood cells (blasts) in the bone marrow and peripheral blood. The two main categories are:
- Acute Lymphoblastic Leukemia (ALL) - Originates from lymphoid progenitor cells, primarily affecting children but can also occur in adults.
- Acute Myeloid Leukemia (AML) - Develops from myeloid progenitor cells and is more common in older adults.

2. Chronic Leukemias - These types of leukemia progress slowly, with symptoms developing over a period of months to years. They involve the production of relatively mature, but still abnormal, white blood cells that can accumulate in large numbers in the bone marrow and peripheral blood. The two main categories are:
- Chronic Lymphocytic Leukemia (CLL) - Affects B-lymphocytes and is more common in older adults.
- Chronic Myeloid Leukemia (CML) - Originates from myeloid progenitor cells, characterized by the presence of a specific genetic abnormality called the Philadelphia chromosome. It can occur at any age but is more common in middle-aged and older adults.

Treatment options for leukemia depend on the type, stage, and individual patient factors. Treatments may include chemotherapy, targeted therapy, immunotherapy, stem cell transplantation, or a combination of these approaches.

Precursor Cell Lymphoblastic Leukemia-Lymphoma (previously known as Precursor T-lymphoblastic Leukemia/Lymphoma) is a type of cancer that affects the early stages of T-cell development. It is a subtype of acute lymphoblastic leukemia (ALL), which is characterized by the overproduction of immature white blood cells called lymphoblasts in the bone marrow, blood, and other organs.

In Precursor Cell Lymphoblastic Leukemia-Lymphoma, these abnormal lymphoblasts accumulate primarily in the lymphoid tissues such as the thymus and lymph nodes, leading to the enlargement of these organs. This subtype is more aggressive than other forms of ALL and has a higher risk of spreading to the central nervous system (CNS).

The medical definition of Precursor Cell Lymphoblastic Leukemia-Lymphoma includes:

1. A malignant neoplasm of immature T-cell precursors, also known as lymphoblasts.
2. Characterized by the proliferation and accumulation of these abnormal cells in the bone marrow, blood, and lymphoid tissues such as the thymus and lymph nodes.
3. Often associated with chromosomal abnormalities, genetic mutations, or aberrant gene expression that contribute to its aggressive behavior and poor prognosis.
4. Typically presents with symptoms related to bone marrow failure (anemia, neutropenia, thrombocytopenia), lymphadenopathy (swollen lymph nodes), hepatosplenomegaly (enlarged liver and spleen), and potential CNS involvement.
5. Diagnosed through a combination of clinical evaluation, imaging studies, and laboratory tests, including bone marrow aspiration and biopsy, immunophenotyping, cytogenetic analysis, and molecular genetic testing.
6. Treated with intensive multi-agent chemotherapy regimens, often combined with radiation therapy and/or stem cell transplantation to achieve remission and improve survival outcomes.

Acute myeloid leukemia (AML) is a type of cancer that originates in the bone marrow, the soft inner part of certain bones where new blood cells are made. In AML, the immature cells, called blasts, in the bone marrow fail to mature into normal blood cells. Instead, these blasts accumulate and interfere with the production of normal blood cells, leading to a shortage of red blood cells (anemia), platelets (thrombocytopenia), and normal white blood cells (leukopenia).

AML is called "acute" because it can progress quickly and become severe within days or weeks without treatment. It is a type of myeloid leukemia, which means that it affects the myeloid cells in the bone marrow. Myeloid cells are a type of white blood cell that includes monocytes and granulocytes, which help fight infection and defend the body against foreign invaders.

In AML, the blasts can build up in the bone marrow and spread to other parts of the body, including the blood, lymph nodes, liver, spleen, and brain. This can cause a variety of symptoms, such as fatigue, fever, frequent infections, easy bruising or bleeding, and weight loss.

AML is typically treated with a combination of chemotherapy, radiation therapy, and/or stem cell transplantation. The specific treatment plan will depend on several factors, including the patient's age, overall health, and the type and stage of the leukemia.

Intranuclear inclusion bodies are abnormal, rounded structures found within the nucleus of a cell. They are composed of aggregated proteins or other cellular components and can be associated with various viral infections and certain genetic disorders. These inclusion bodies can interfere with normal nuclear functions, leading to cell damage and contributing to the pathogenesis of diseases such as cytomegalovirus infection, rabies, and some forms of neurodegenerative disorders like polyglutamine diseases. The presence of intranuclear inclusion bodies is often used in diagnostic pathology to help identify specific underlying conditions.

Chronic lymphocytic leukemia (CLL) is a type of cancer that starts from cells that become certain white blood cells (called lymphocytes) in the bone marrow. The cancer (leukemia) cells start in the bone marrow but then go into the blood.

In CLL, the leukemia cells often build up slowly. Many people don't have any symptoms for at least a few years. But over time, the cells can spread to other parts of the body, including the lymph nodes, liver, and spleen.

The "B-cell" part of the name refers to the fact that the cancer starts in a type of white blood cell called a B lymphocyte or B cell. The "chronic" part means that this leukemia usually progresses more slowly than other types of leukemia.

It's important to note that chronic lymphocytic leukemia is different from chronic myelogenous leukemia (CML). Although both are cancers of the white blood cells, they start in different types of white blood cells and progress differently.

Leukemia, B-cell is a type of cancer that affects the blood and bone marrow, characterized by an overproduction of abnormal B-lymphocytes, a type of white blood cell. These abnormal cells accumulate in the bone marrow and interfere with the production of normal blood cells, leading to anemia, infection, and bleeding.

B-cells are a type of lymphocyte that plays a crucial role in the immune system by producing antibodies to help fight off infections. In B-cell leukemia, the cancerous B-cells do not mature properly and accumulate in the bone marrow, leading to a decrease in the number of healthy white blood cells, red blood cells, and platelets.

There are several types of B-cell leukemia, including acute lymphoblastic leukemia (ALL) and chronic lymphocytic leukemia (CLL). ALL is more common in children and young adults, while CLL is more common in older adults. Treatment options for B-cell leukemia depend on the type and stage of the disease and may include chemotherapy, radiation therapy, stem cell transplantation, or targeted therapies.

Tumor suppressor proteins are a type of regulatory protein that helps control the cell cycle and prevent cells from dividing and growing in an uncontrolled manner. They work to inhibit tumor growth by preventing the formation of tumors or slowing down their progression. These proteins can repair damaged DNA, regulate gene expression, and initiate programmed cell death (apoptosis) if the damage is too severe for repair.

Mutations in tumor suppressor genes, which provide the code for these proteins, can lead to a decrease or loss of function in the resulting protein. This can result in uncontrolled cell growth and division, leading to the formation of tumors and cancer. Examples of tumor suppressor proteins include p53, Rb (retinoblastoma), and BRCA1/2.

Experimental leukemia refers to the stage of research or clinical trials where new therapies, treatments, or diagnostic methods are being studied for leukemia. Leukemia is a type of cancer that affects the blood and bone marrow, leading to an overproduction of abnormal white blood cells.

In the experimental stage, researchers investigate various aspects of leukemia, such as its causes, progression, and potential treatments. They may conduct laboratory studies using cell cultures or animal models to understand the disease better and test new therapeutic approaches. Additionally, clinical trials may be conducted to evaluate the safety and efficacy of novel treatments in human patients with leukemia.

Experimental research in leukemia is crucial for advancing our understanding of the disease and developing more effective treatment strategies. It involves a rigorous and systematic process that adheres to ethical guidelines and scientific standards to ensure the validity and reliability of the findings.

Nuclear proteins are a category of proteins that are primarily found in the nucleus of a eukaryotic cell. They play crucial roles in various nuclear functions, such as DNA replication, transcription, repair, and RNA processing. This group includes structural proteins like lamins, which form the nuclear lamina, and regulatory proteins, such as histones and transcription factors, that are involved in gene expression. Nuclear localization signals (NLS) often help target these proteins to the nucleus by interacting with importin proteins during active transport across the nuclear membrane.

The Myeloid-Lymphoid Leukemia (MLL) protein, also known as MLL1 or HRX, is a histone methyltransferase that plays a crucial role in the regulation of gene expression. It is involved in various cellular processes, including embryonic development and hematopoiesis (the formation of blood cells).

The MLL protein is encoded by the MLL gene, which is located on chromosome 11q23. This gene is frequently rearranged or mutated in certain types of leukemia, leading to the production of abnormal fusion proteins that contribute to tumor development and progression. These MLL-rearranged leukemias are aggressive and have a poor prognosis, making them an important area of research in the field of oncology.

The cell nucleus is a membrane-bound organelle found in the eukaryotic cells (cells with a true nucleus). It contains most of the cell's genetic material, organized as DNA molecules bound to hist proteins, forming chromosomes. The nuclear membrane, also known as the nuclear envelope, consists of two lipid bilayers perforated by nuclear pores that regulate the transport of molecules between the nucleus and the cytoplasm.

The cell nucleus has several structures with essential functions:

1. Chromosomes: These are thread-like structures made up of DNA, hist proteins, and RNA. They carry genetic information in the form of genes and are responsible for inheritance.
2. Nucleolus: A prominent structure within the nucleus, the nucleolus is the site of ribosome biogenesis. It assembles ribosomal subunits, which are then transported to the cytoplasm for protein synthesis.
3. Nuclear matrix/nuclear lamina: A network of proteins that provides structural support and anchorage for chromosomes, the nucleolus, and other nuclear components. It is located directly inside the inner nuclear membrane.
4. Nuclear pores: These are large protein complexes embedded in the nuclear membrane that regulate the exchange of molecules between the nucleus and cytoplasm. They allow the passage of ions, small molecules, and proteins while preventing the uncontrolled release of genetic material.
5. Heterochromatin and euchromatin: These are different forms of chromatin (chromosomal material) with distinct functions. Heterochromatin is highly condensed and transcriptionally inactive, whereas euchromatin is less condensed and more accessible for gene transcription.

Together, these structures within the cell nucleus play crucial roles in maintaining genome stability, regulating gene expression, and ensuring proper cell function.

Transcription factors are proteins that play a crucial role in regulating gene expression by controlling the transcription of DNA to messenger RNA (mRNA). They function by binding to specific DNA sequences, known as response elements, located in the promoter region or enhancer regions of target genes. This binding can either activate or repress the initiation of transcription, depending on the properties and interactions of the particular transcription factor. Transcription factors often act as part of a complex network of regulatory proteins that determine the precise spatiotemporal patterns of gene expression during development, differentiation, and homeostasis in an organism.

Leukemia, myeloid is a type of cancer that originates in the bone marrow, where blood cells are produced. Myeloid leukemia affects the myeloid cells, which include red blood cells, platelets, and most types of white blood cells. In this condition, the bone marrow produces abnormal myeloid cells that do not mature properly and accumulate in the bone marrow and blood. These abnormal cells hinder the production of normal blood cells, leading to various symptoms such as anemia, fatigue, increased risk of infections, and easy bruising or bleeding.

There are several types of myeloid leukemias, including acute myeloid leukemia (AML) and chronic myeloid leukemia (CML). AML progresses rapidly and requires immediate treatment, while CML tends to progress more slowly. The exact causes of myeloid leukemia are not fully understood, but risk factors include exposure to radiation or certain chemicals, smoking, genetic disorders, and a history of chemotherapy or other cancer treatments.

A neoplasm is a tumor or growth that is formed by an abnormal and excessive proliferation of cells, which can be benign or malignant. Neoplasm proteins are therefore any proteins that are expressed or produced in these neoplastic cells. These proteins can play various roles in the development, progression, and maintenance of neoplasms.

Some neoplasm proteins may contribute to the uncontrolled cell growth and division seen in cancer, such as oncogenic proteins that promote cell cycle progression or inhibit apoptosis (programmed cell death). Others may help the neoplastic cells evade the immune system, allowing them to proliferate undetected. Still others may be involved in angiogenesis, the formation of new blood vessels that supply the tumor with nutrients and oxygen.

Neoplasm proteins can also serve as biomarkers for cancer diagnosis, prognosis, or treatment response. For example, the presence or level of certain neoplasm proteins in biological samples such as blood or tissue may indicate the presence of a specific type of cancer, help predict the likelihood of cancer recurrence, or suggest whether a particular therapy will be effective.

Overall, understanding the roles and behaviors of neoplasm proteins can provide valuable insights into the biology of cancer and inform the development of new diagnostic and therapeutic strategies.

A blast crisis is a severe and life-threatening complication that can occur in patients with certain types of blood cancer, such as chronic myelogenous leukemia (CML) or acute lymphoblastic leukemia (ALL). It is characterized by the rapid growth and accumulation of immature blood cells, known as blasts, in the bone marrow and peripheral blood.

In a blast crisis, the blasts crowd out normal blood-forming cells in the bone marrow, leading to a significant decrease in the production of healthy red blood cells, white blood cells, and platelets. This can result in symptoms such as anemia, fatigue, infection, easy bruising or bleeding, and an enlarged spleen.

Blast crisis is often treated with aggressive chemotherapy, targeted therapy, or stem cell transplantation to eliminate the abnormal blasts and restore normal blood cell production. The prognosis for patients in blast crisis can be poor, depending on the type of leukemia, the patient's age and overall health, and the response to treatment.

An acute disease is a medical condition that has a rapid onset, develops quickly, and tends to be short in duration. Acute diseases can range from minor illnesses such as a common cold or flu, to more severe conditions such as pneumonia, meningitis, or a heart attack. These types of diseases often have clear symptoms that are easy to identify, and they may require immediate medical attention or treatment.

Acute diseases are typically caused by an external agent or factor, such as a bacterial or viral infection, a toxin, or an injury. They can also be the result of a sudden worsening of an existing chronic condition. In general, acute diseases are distinct from chronic diseases, which are long-term medical conditions that develop slowly over time and may require ongoing management and treatment.

Examples of acute diseases include:

* Acute bronchitis: a sudden inflammation of the airways in the lungs, often caused by a viral infection.
* Appendicitis: an inflammation of the appendix that can cause severe pain and requires surgical removal.
* Gastroenteritis: an inflammation of the stomach and intestines, often caused by a viral or bacterial infection.
* Migraine headaches: intense headaches that can last for hours or days, and are often accompanied by nausea, vomiting, and sensitivity to light and sound.
* Myocardial infarction (heart attack): a sudden blockage of blood flow to the heart muscle, often caused by a buildup of plaque in the coronary arteries.
* Pneumonia: an infection of the lungs that can cause coughing, chest pain, and difficulty breathing.
* Sinusitis: an inflammation of the sinuses, often caused by a viral or bacterial infection.

It's important to note that while some acute diseases may resolve on their own with rest and supportive care, others may require medical intervention or treatment to prevent complications and promote recovery. If you are experiencing symptoms of an acute disease, it is always best to seek medical attention to ensure proper diagnosis and treatment.

Bone marrow is the spongy tissue found inside certain bones in the body, such as the hips, thighs, and vertebrae. It is responsible for producing blood-forming cells, including red blood cells, white blood cells, and platelets. There are two types of bone marrow: red marrow, which is involved in blood cell production, and yellow marrow, which contains fatty tissue.

Red bone marrow contains hematopoietic stem cells, which can differentiate into various types of blood cells. These stem cells continuously divide and mature to produce new blood cells that are released into the circulation. Red blood cells carry oxygen throughout the body, white blood cells help fight infections, and platelets play a crucial role in blood clotting.

Bone marrow also serves as a site for immune cell development and maturation. It contains various types of immune cells, such as lymphocytes, macrophages, and dendritic cells, which help protect the body against infections and diseases.

Abnormalities in bone marrow function can lead to several medical conditions, including anemia, leukopenia, thrombocytopenia, and various types of cancer, such as leukemia and multiple myeloma. Bone marrow aspiration and biopsy are common diagnostic procedures used to evaluate bone marrow health and function.

'Tumor cells, cultured' refers to the process of removing cancerous cells from a tumor and growing them in controlled laboratory conditions. This is typically done by isolating the tumor cells from a patient's tissue sample, then placing them in a nutrient-rich environment that promotes their growth and multiplication.

The resulting cultured tumor cells can be used for various research purposes, including the study of cancer biology, drug development, and toxicity testing. They provide a valuable tool for researchers to better understand the behavior and characteristics of cancer cells outside of the human body, which can lead to the development of more effective cancer treatments.

It is important to note that cultured tumor cells may not always behave exactly the same way as they do in the human body, so findings from cell culture studies must be validated through further research, such as animal models or clinical trials.

Remission induction is a treatment approach in medicine, particularly in the field of oncology and hematology. It refers to the initial phase of therapy aimed at reducing or eliminating the signs and symptoms of active disease, such as cancer or autoimmune disorders. The primary goal of remission induction is to achieve a complete response (disappearance of all detectable signs of the disease) or a partial response (a decrease in the measurable extent of the disease). This phase of treatment is often intensive and may involve the use of multiple drugs or therapies, including chemotherapy, immunotherapy, or targeted therapy. After remission induction, patients may receive additional treatments to maintain the remission and prevent relapse, known as consolidation or maintenance therapy.

SUMO-1 (Small Ubiquitin-like Modifier 1) protein is a member of the SUMO family of post-translational modifiers, which are involved in the regulation of various cellular processes such as nuclear-cytoplasmic transport, transcriptional regulation, and DNA repair. The SUMO-1 protein is covalently attached to specific lysine residues on target proteins through a process called sumoylation, which can alter the activity, localization, or stability of the modified protein. Sumoylation plays a crucial role in maintaining cellular homeostasis and has been implicated in several human diseases, including cancer and neurodegenerative disorders.

Acute Promyelocytic Leukemia (APL) is a specific subtype of acute myeloid leukemia (AML), a cancer of the blood and bone marrow. It is characterized by the accumulation of abnormal promyelocytes, which are immature white blood cells, in the bone marrow and blood. These abnormal cells are produced due to a genetic mutation that involves the retinoic acid receptor alpha (RARA) gene on chromosome 17, often as a result of a translocation with the promyelocytic leukemia (PML) gene on chromosome 15 [t(15;17)]. This genetic alteration disrupts the normal differentiation and maturation process of the promyelocytes, leading to their uncontrolled proliferation and impaired function.

APL typically presents with symptoms related to decreased blood cell production, such as anemia (fatigue, weakness, shortness of breath), thrombocytopenia (easy bruising, bleeding, or petechiae), and neutropenia (increased susceptibility to infections). Additionally, APL is often associated with a high risk of disseminated intravascular coagulation (DIC), a serious complication characterized by abnormal blood clotting and bleeding.

The treatment for Acute Promyelocytic Leukemia typically involves a combination of chemotherapy and all-trans retinoic acid (ATRA) or arsenic trioxide (ATO) therapy, which target the specific genetic alteration in APL cells. This approach has significantly improved the prognosis for patients with this disease, with many achieving long-term remission and even cures.

I'm sorry for any confusion, but "oxides" is not a term that has a specific medical definition. Oxides are a class of chemical compounds that contain at least one oxygen atom and one other element. They can be formed through the process of oxidation, which involves the combination of oxygen with another substance.

In a broader sense, you might encounter the term "oxide" in a medical context when discussing various materials or substances used in medical devices, treatments, or research. For instance, titanium dioxide is a common ingredient in medical-grade sunscreens due to its ability to block and scatter UV light. However, it's important to note that the term "oxides" itself doesn't have a direct connection to medicine or human health.

Arsenicals are a group of chemicals that contain arsenic, a naturally occurring element that is toxic to humans and animals. Arsenic can combine with other elements such as chlorine, sulfur, or carbon to form various inorganic and organic compounds known as arsenicals. These compounds have been used in a variety of industrial and agricultural applications, including wood preservatives, pesticides, and herbicides.

Exposure to high levels of arsenic can cause serious health effects, including skin damage, circulatory problems, and increased risk of cancer. Long-term exposure to lower levels of arsenic can also lead to chronic health issues, such as neurological damage and diabetes. Therefore, the use of arsenicals is regulated in many countries to minimize human and environmental exposure.

Lymphocytes are a type of white blood cell that is an essential part of the immune system. They are responsible for recognizing and responding to potentially harmful substances such as viruses, bacteria, and other foreign invaders. There are two main types of lymphocytes: B-lymphocytes (B-cells) and T-lymphocytes (T-cells).

B-lymphocytes produce antibodies, which are proteins that help to neutralize or destroy foreign substances. When a B-cell encounters a foreign substance, it becomes activated and begins to divide and differentiate into plasma cells, which produce and secrete large amounts of antibodies. These antibodies bind to the foreign substance, marking it for destruction by other immune cells.

T-lymphocytes, on the other hand, are involved in cell-mediated immunity. They directly attack and destroy infected cells or cancerous cells. T-cells can also help to regulate the immune response by producing chemical signals that activate or inhibit other immune cells.

Lymphocytes are produced in the bone marrow and mature in either the bone marrow (B-cells) or the thymus gland (T-cells). They circulate throughout the body in the blood and lymphatic system, where they can be found in high concentrations in lymph nodes, the spleen, and other lymphoid organs.

Abnormalities in the number or function of lymphocytes can lead to a variety of immune-related disorders, including immunodeficiency diseases, autoimmune disorders, and cancer.

Chronic myelogenous leukemia (CML), BCR-ABL positive is a specific subtype of leukemia that originates in the bone marrow and involves the excessive production of mature granulocytes, a type of white blood cell. It is characterized by the presence of the Philadelphia chromosome, which is formed by a genetic translocation between chromosomes 9 and 22, resulting in the formation of the BCR-ABL fusion gene. This gene encodes for an abnormal protein with increased tyrosine kinase activity, leading to uncontrolled cell growth and division. The presence of this genetic abnormality is used to confirm the diagnosis and guide treatment decisions.

The cell nucleus is a membrane-bound organelle found in the eukaryotic cells (cells with a true nucleus). It contains most of the cell's genetic material, organized as DNA molecules in complex with proteins, RNA molecules, and histones to form chromosomes.

The primary function of the cell nucleus is to regulate and control the activities of the cell, including growth, metabolism, protein synthesis, and reproduction. It also plays a crucial role in the process of mitosis (cell division) by separating and protecting the genetic material during this process. The nuclear membrane, or nuclear envelope, surrounding the nucleus is composed of two lipid bilayers with numerous pores that allow for the selective transport of molecules between the nucleoplasm (nucleus interior) and the cytoplasm (cell exterior).

The cell nucleus is a vital structure in eukaryotic cells, and its dysfunction can lead to various diseases, including cancer and genetic disorders.

Polymerase Chain Reaction (PCR) is a laboratory technique used to amplify specific regions of DNA. It enables the production of thousands to millions of copies of a particular DNA sequence in a rapid and efficient manner, making it an essential tool in various fields such as molecular biology, medical diagnostics, forensic science, and research.

The PCR process involves repeated cycles of heating and cooling to separate the DNA strands, allow primers (short sequences of single-stranded DNA) to attach to the target regions, and extend these primers using an enzyme called Taq polymerase, resulting in the exponential amplification of the desired DNA segment.

In a medical context, PCR is often used for detecting and quantifying specific pathogens (viruses, bacteria, fungi, or parasites) in clinical samples, identifying genetic mutations or polymorphisms associated with diseases, monitoring disease progression, and evaluating treatment effectiveness.

Medical Definition:

Murine leukemia virus (MLV) is a type of retrovirus that primarily infects and causes various types of malignancies such as leukemias and lymphomas in mice. It is a complex genus of viruses, with many strains showing different pathogenic properties.

MLV contains two identical single-stranded RNA genomes and has the ability to reverse transcribe its RNA into DNA upon infection, integrating this proviral DNA into the host cell's genome. This is facilitated by an enzyme called reverse transcriptase, which MLV carries within its viral particle.

The virus can be horizontally transmitted between mice through close contact with infected saliva, urine, or milk. Vertical transmission from mother to offspring can also occur either in-utero or through the ingestion of infected breast milk.

MLV has been extensively studied as a model system for retroviral pathogenesis and tumorigenesis, contributing significantly to our understanding of oncogenes and their role in cancer development. It's important to note that Murine Leukemia Virus does not infect humans.

A cell line is a culture of cells that are grown in a laboratory for use in research. These cells are usually taken from a single cell or group of cells, and they are able to divide and grow continuously in the lab. Cell lines can come from many different sources, including animals, plants, and humans. They are often used in scientific research to study cellular processes, disease mechanisms, and to test new drugs or treatments. Some common types of human cell lines include HeLa cells (which come from a cancer patient named Henrietta Lacks), HEK293 cells (which come from embryonic kidney cells), and HUVEC cells (which come from umbilical vein endothelial cells). It is important to note that cell lines are not the same as primary cells, which are cells that are taken directly from a living organism and have not been grown in the lab.

Leukemia, T-cell is a type of cancer that affects the T-cells or T-lymphocytes, which are a type of white blood cells responsible for cell-mediated immunity. It is characterized by an excessive and uncontrolled production of abnormal T-cells in the bone marrow, leading to the displacement of healthy cells and impairing the body's ability to fight infections and regulate immune responses.

T-cell leukemia can be acute or chronic, depending on the rate at which the disease progresses. Acute T-cell leukemia progresses rapidly, while chronic T-cell leukemia has a slower course of progression. Symptoms may include fatigue, fever, frequent infections, weight loss, easy bruising or bleeding, and swollen lymph nodes. Treatment typically involves chemotherapy, radiation therapy, stem cell transplantation, or targeted therapy, depending on the type and stage of the disease.

Acute Monocytic Leukemia (AML-M5) is a subtype of acute myeloid leukemia (AML), which is a type of cancer affecting the blood and bone marrow. In AML-M5, there is an overproduction of abnormal monocytes, a type of white blood cell that normally helps fight infection and is involved in the body's immune response. These abnormal monocytes accumulate in the bone marrow and interfere with the production of normal blood cells, leading to symptoms such as fatigue, frequent infections, and easy bruising or bleeding. The disease progresses rapidly without treatment, making it crucial to begin therapy as soon as possible after diagnosis.

HeLa cells are a type of immortalized cell line used in scientific research. They are derived from a cancer that developed in the cervical tissue of Henrietta Lacks, an African-American woman, in 1951. After her death, cells taken from her tumor were found to be capable of continuous division and growth in a laboratory setting, making them an invaluable resource for medical research.

HeLa cells have been used in a wide range of scientific studies, including research on cancer, viruses, genetics, and drug development. They were the first human cell line to be successfully cloned and are able to grow rapidly in culture, doubling their population every 20-24 hours. This has made them an essential tool for many areas of biomedical research.

It is important to note that while HeLa cells have been instrumental in numerous scientific breakthroughs, the story of their origin raises ethical questions about informed consent and the use of human tissue in research.

The Moloney murine leukemia virus (Mo-MLV) is a type of retrovirus, specifically a gammaretrovirus, that is commonly found in mice. It was first discovered and isolated by John Moloney in 1960. Mo-MLV is known to cause various types of cancerous conditions, particularly leukemia, in susceptible mouse strains.

Mo-MLV has a single-stranded RNA genome that is reverse transcribed into double-stranded DNA upon infection of the host cell. This viral DNA then integrates into the host's genome and utilizes the host's cellular machinery to produce new virus particles. The Mo-MLV genome encodes for several viral proteins, including gag (group-specific antigen), pol (polymerase), and env (envelope) proteins, which are essential for the replication cycle of the virus.

Mo-MLV is widely used in laboratory research as a model retrovirus to study various aspects of viral replication, gene therapy, and oncogenesis. It has also been engineered as a vector for gene delivery applications due to its ability to efficiently integrate into the host genome and deliver large DNA sequences. However, it is important to note that Mo-MLV and other retroviruses have the potential to cause insertional mutagenesis, which can lead to unintended genetic alterations and adverse effects in some cases.

Nuclear antigens are proteins or other molecules found in the nucleus of a cell that can stimulate an immune response and produce antibodies when they are recognized as foreign by the body's immune system. These antigens are normally located inside the cell and are not typically exposed to the immune system, but under certain circumstances, such as during cell death or damage, they may be released and become targets of the immune system.

Nuclear antigens can play a role in the development of some autoimmune diseases, such as systemic lupus erythematosus (SLE), where the body's immune system mistakenly attacks its own cells and tissues. In SLE, nuclear antigens such as double-stranded DNA and nucleoproteins are common targets of the abnormal immune response.

Testing for nuclear antigens is often used in the diagnosis and monitoring of autoimmune diseases. For example, a positive test for anti-double-stranded DNA antibodies is a specific indicator of SLE and can help confirm the diagnosis. However, it's important to note that not all people with SLE will have positive nuclear antigen tests, and other factors must also be considered in making a diagnosis.

Zinc fingers are a type of protein structural motif involved in specific DNA binding and, by extension, in the regulation of gene expression. They are so named because of their characteristic "finger-like" shape that is formed when a zinc ion binds to the amino acids within the protein. This structure allows the protein to interact with and recognize specific DNA sequences, thereby playing a crucial role in various biological processes such as transcription, repair, and recombination of genetic material.

DNA-binding proteins are a type of protein that have the ability to bind to DNA (deoxyribonucleic acid), the genetic material of organisms. These proteins play crucial roles in various biological processes, such as regulation of gene expression, DNA replication, repair and recombination.

The binding of DNA-binding proteins to specific DNA sequences is mediated by non-covalent interactions, including electrostatic, hydrogen bonding, and van der Waals forces. The specificity of binding is determined by the recognition of particular nucleotide sequences or structural features of the DNA molecule.

DNA-binding proteins can be classified into several categories based on their structure and function, such as transcription factors, histones, and restriction enzymes. Transcription factors are a major class of DNA-binding proteins that regulate gene expression by binding to specific DNA sequences in the promoter region of genes and recruiting other proteins to modulate transcription. Histones are DNA-binding proteins that package DNA into nucleosomes, the basic unit of chromatin structure. Restriction enzymes are DNA-binding proteins that recognize and cleave specific DNA sequences, and are widely used in molecular biology research and biotechnology applications.

Hairy cell leukemia (HCL) is a rare, slow-growing type of cancer in which the bone marrow makes too many B cells (a type of white blood cell). These excess B cells are often referred to as "hairy cells" because they look abnormal under the microscope, with fine projections or "hair-like" cytoplasmic protrusions.

In HCL, these abnormal B cells can build up in the bone marrow and spleen, causing both of them to enlarge. The accumulation of hairy cells in the bone marrow can crowd out healthy blood cells, leading to a shortage of red blood cells (anemia), platelets (thrombocytopenia), and normal white blood cells (leukopenia). This can result in fatigue, increased risk of infection, and easy bruising or bleeding.

HCL is typically an indolent disease, meaning that it progresses slowly over time. However, some cases may require treatment to manage symptoms and prevent complications. Treatment options for HCL include chemotherapy, immunotherapy, targeted therapy, and stem cell transplantation. Regular follow-up with a healthcare provider is essential to monitor the disease's progression and adjust treatment plans as needed.

Protein binding, in the context of medical and biological sciences, refers to the interaction between a protein and another molecule (known as the ligand) that results in a stable complex. This process is often reversible and can be influenced by various factors such as pH, temperature, and concentration of the involved molecules.

In clinical chemistry, protein binding is particularly important when it comes to drugs, as many of them bind to proteins (especially albumin) in the bloodstream. The degree of protein binding can affect a drug's distribution, metabolism, and excretion, which in turn influence its therapeutic effectiveness and potential side effects.

Protein-bound drugs may be less available for interaction with their target tissues, as only the unbound or "free" fraction of the drug is active. Therefore, understanding protein binding can help optimize dosing regimens and minimize adverse reactions.

Leukemia L1210 is not a medical definition itself, but it refers to a specific mouse leukemia cell line that was established in 1948. These cells are a type of acute myeloid leukemia (AML) and have been widely used in cancer research as a model for studying the disease, testing new therapies, and understanding the biology of leukemia. The L1210 cell line has contributed significantly to the development of various chemotherapeutic agents and treatment strategies for leukemia and other cancers.

Tertiary protein structure refers to the three-dimensional arrangement of all the elements (polypeptide chains) of a single protein molecule. It is the highest level of structural organization and results from interactions between various side chains (R groups) of the amino acids that make up the protein. These interactions, which include hydrogen bonds, ionic bonds, van der Waals forces, and disulfide bridges, give the protein its unique shape and stability, which in turn determines its function. The tertiary structure of a protein can be stabilized by various factors such as temperature, pH, and the presence of certain ions. Any changes in these factors can lead to denaturation, where the protein loses its tertiary structure and thus its function.

Transcriptional activation is the process by which a cell increases the rate of transcription of specific genes from DNA to RNA. This process is tightly regulated and plays a crucial role in various biological processes, including development, differentiation, and response to environmental stimuli.

Transcriptional activation occurs when transcription factors (proteins that bind to specific DNA sequences) interact with the promoter region of a gene and recruit co-activator proteins. These co-activators help to remodel the chromatin structure around the gene, making it more accessible for the transcription machinery to bind and initiate transcription.

Transcriptional activation can be regulated at multiple levels, including the availability and activity of transcription factors, the modification of histone proteins, and the recruitment of co-activators or co-repressors. Dysregulation of transcriptional activation has been implicated in various diseases, including cancer and genetic disorders.

Fluorescence microscopy is a type of microscopy that uses fluorescent dyes or proteins to highlight and visualize specific components within a sample. In this technique, the sample is illuminated with high-energy light, typically ultraviolet (UV) or blue light, which excites the fluorescent molecules causing them to emit lower-energy, longer-wavelength light, usually visible light in the form of various colors. This emitted light is then collected by the microscope and detected to produce an image.

Fluorescence microscopy has several advantages over traditional brightfield microscopy, including the ability to visualize specific structures or molecules within a complex sample, increased sensitivity, and the potential for quantitative analysis. It is widely used in various fields of biology and medicine, such as cell biology, neuroscience, and pathology, to study the structure, function, and interactions of cells and proteins.

There are several types of fluorescence microscopy techniques, including widefield fluorescence microscopy, confocal microscopy, two-photon microscopy, and total internal reflection fluorescence (TIRF) microscopy, each with its own strengths and limitations. These techniques can provide valuable insights into the behavior of cells and proteins in health and disease.

Bovine Leukemia Virus (BLV) is a retrovirus that infects cattle and causes enzootic bovine leukosis, a neoplastic disease characterized by the proliferation of malignant B-lymphocytes. The virus primarily targets the animal's immune system, leading to a decrease in the number of white blood cells (leukopenia) and an increased susceptibility to other infections.

The virus is transmitted horizontally through close contact with infected animals or vertically from mother to offspring via infected milk or colostrum. The majority of BLV-infected cattle remain asymptomatic carriers, but a small percentage develop clinical signs such as lymphoma, weight loss, and decreased milk production.

BLV is closely related to human T-cell leukemia virus (HTLV), and both viruses belong to the Retroviridae family, genus Deltaretrovirus. However, it's important to note that BLV does not cause leukemia or any other neoplastic diseases in humans.

Feline Leukemia Virus (FeLV) is a retrovirus that primarily infects cats, causing a variety of diseases and disorders. It is the causative agent of feline leukemia, a name given to a syndrome characterized by a variety of symptoms such as lymphoma (cancer of the lymphatic system), anemia, immunosuppression, and reproductive disorders. FeLV is typically transmitted through close contact with infected cats, such as through saliva, nasal secretions, urine, and milk. It can also be spread through shared litter boxes and feeding dishes.

FeLV infects cells of the immune system, leading to a weakened immune response and making the cat more susceptible to other infections. The virus can also integrate its genetic material into the host's DNA, potentially causing cancerous changes in infected cells. FeLV is a significant health concern for cats, particularly those that are exposed to outdoor environments or come into contact with other cats. Vaccination and regular veterinary care can help protect cats from this virus.

A cell line that is derived from tumor cells and has been adapted to grow in culture. These cell lines are often used in research to study the characteristics of cancer cells, including their growth patterns, genetic changes, and responses to various treatments. They can be established from many different types of tumors, such as carcinomas, sarcomas, and leukemias. Once established, these cell lines can be grown and maintained indefinitely in the laboratory, allowing researchers to conduct experiments and studies that would not be feasible using primary tumor cells. It is important to note that tumor cell lines may not always accurately represent the behavior of the original tumor, as they can undergo genetic changes during their time in culture.

Apoptosis is a programmed and controlled cell death process that occurs in multicellular organisms. It is a natural process that helps maintain tissue homeostasis by eliminating damaged, infected, or unwanted cells. During apoptosis, the cell undergoes a series of morphological changes, including cell shrinkage, chromatin condensation, and fragmentation into membrane-bound vesicles called apoptotic bodies. These bodies are then recognized and engulfed by neighboring cells or phagocytic cells, preventing an inflammatory response. Apoptosis is regulated by a complex network of intracellular signaling pathways that involve proteins such as caspases, Bcl-2 family members, and inhibitors of apoptosis (IAPs).

Genetic transcription is the process by which the information in a strand of DNA is used to create a complementary RNA molecule. This process is the first step in gene expression, where the genetic code in DNA is converted into a form that can be used to produce proteins or functional RNAs.

During transcription, an enzyme called RNA polymerase binds to the DNA template strand and reads the sequence of nucleotide bases. As it moves along the template, it adds complementary RNA nucleotides to the growing RNA chain, creating a single-stranded RNA molecule that is complementary to the DNA template strand. Once transcription is complete, the RNA molecule may undergo further processing before it can be translated into protein or perform its functional role in the cell.

Transcription can be either "constitutive" or "regulated." Constitutive transcription occurs at a relatively constant rate and produces essential proteins that are required for basic cellular functions. Regulated transcription, on the other hand, is subject to control by various intracellular and extracellular signals, allowing cells to respond to changing environmental conditions or developmental cues.

An oncogene protein fusion is a result of a genetic alteration in which parts of two different genes combine to create a hybrid gene that can contribute to the development of cancer. This fusion can lead to the production of an abnormal protein that promotes uncontrolled cell growth and division, ultimately resulting in a malignant tumor. Oncogene protein fusions are often caused by chromosomal rearrangements such as translocations, inversions, or deletions and are commonly found in various types of cancer, including leukemia and sarcoma. These genetic alterations can serve as potential targets for cancer diagnosis and therapy.

Gene expression regulation in leukemia refers to the processes that control the production or activation of specific proteins encoded by genes in leukemic cells. These regulatory mechanisms include various molecular interactions that can either promote or inhibit gene transcription and translation. In leukemia, abnormal gene expression regulation can lead to uncontrolled proliferation, differentiation arrest, and accumulation of malignant white blood cells (leukemia cells) in the bone marrow and peripheral blood.

Dysregulated gene expression in leukemia may involve genetic alterations such as mutations, chromosomal translocations, or epigenetic changes that affect DNA methylation patterns and histone modifications. These changes can result in the overexpression of oncogenes (genes with cancer-promoting functions) or underexpression of tumor suppressor genes (genes that prevent uncontrolled cell growth).

Understanding gene expression regulation in leukemia is crucial for developing targeted therapies and improving diagnostic, prognostic, and treatment strategies.

Transfection is a term used in molecular biology that refers to the process of deliberately introducing foreign genetic material (DNA, RNA or artificial gene constructs) into cells. This is typically done using chemical or physical methods, such as lipofection or electroporation. Transfection is widely used in research and medical settings for various purposes, including studying gene function, producing proteins, developing gene therapies, and creating genetically modified organisms. It's important to note that transfection is different from transduction, which is the process of introducing genetic material into cells using viruses as vectors.

Radiation-induced leukemia is a type of cancer that affects the blood-forming tissues of the body, such as the bone marrow. It is caused by exposure to high levels of radiation, which can damage the DNA of cells and lead to their uncontrolled growth and division.

There are several types of radiation-induced leukemia, depending on the specific type of blood cell that becomes cancerous. The most common types are acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL). These forms of leukemia tend to progress quickly and require prompt treatment.

Radiation-induced leukemia is a rare complication of radiation therapy, which is used to treat many types of cancer. The risk of developing this type of leukemia increases with the dose and duration of radiation exposure. It is important to note that the benefits of radiation therapy in treating cancer generally outweigh the small increased risk of developing radiation-induced leukemia.

Symptoms of radiation-induced leukemia may include fatigue, fever, frequent infections, easy bruising or bleeding, and weight loss. If you have been exposed to high levels of radiation and are experiencing these symptoms, it is important to seek medical attention promptly. A diagnosis of radiation-induced leukemia is typically made through a combination of physical exam, medical history, and laboratory tests, such as blood counts and bone marrow biopsy. Treatment may include chemotherapy, radiation therapy, and/or stem cell transplantation.

Recombinant fusion proteins are artificially created biomolecules that combine the functional domains or properties of two or more different proteins into a single protein entity. They are generated through recombinant DNA technology, where the genes encoding the desired protein domains are linked together and expressed as a single, chimeric gene in a host organism, such as bacteria, yeast, or mammalian cells.

The resulting fusion protein retains the functional properties of its individual constituent proteins, allowing for novel applications in research, diagnostics, and therapeutics. For instance, recombinant fusion proteins can be designed to enhance protein stability, solubility, or immunogenicity, making them valuable tools for studying protein-protein interactions, developing targeted therapies, or generating vaccines against infectious diseases or cancer.

Examples of recombinant fusion proteins include:

1. Etaglunatide (ABT-523): A soluble Fc fusion protein that combines the heavy chain fragment crystallizable region (Fc) of an immunoglobulin with the extracellular domain of the human interleukin-6 receptor (IL-6R). This fusion protein functions as a decoy receptor, neutralizing IL-6 and its downstream signaling pathways in rheumatoid arthritis.
2. Etanercept (Enbrel): A soluble TNF receptor p75 Fc fusion protein that binds to tumor necrosis factor-alpha (TNF-α) and inhibits its proinflammatory activity, making it a valuable therapeutic option for treating autoimmune diseases like rheumatoid arthritis, ankylosing spondylitis, and psoriasis.
3. Abatacept (Orencia): A fusion protein consisting of the extracellular domain of cytotoxic T-lymphocyte antigen 4 (CTLA-4) linked to the Fc region of an immunoglobulin, which downregulates T-cell activation and proliferation in autoimmune diseases like rheumatoid arthritis.
4. Belimumab (Benlysta): A monoclonal antibody that targets B-lymphocyte stimulator (BLyS) protein, preventing its interaction with the B-cell surface receptor and inhibiting B-cell activation in systemic lupus erythematosus (SLE).
5. Romiplostim (Nplate): A fusion protein consisting of a thrombopoietin receptor agonist peptide linked to an immunoglobulin Fc region, which stimulates platelet production in patients with chronic immune thrombocytopenia (ITP).
6. Darbepoetin alfa (Aranesp): A hyperglycosylated erythropoiesis-stimulating protein that functions as a longer-acting form of recombinant human erythropoietin, used to treat anemia in patients with chronic kidney disease or cancer.
7. Palivizumab (Synagis): A monoclonal antibody directed against the F protein of respiratory syncytial virus (RSV), which prevents RSV infection and is administered prophylactically to high-risk infants during the RSV season.
8. Ranibizumab (Lucentis): A recombinant humanized monoclonal antibody fragment that binds and inhibits vascular endothelial growth factor A (VEGF-A), used in the treatment of age-related macular degeneration, diabetic retinopathy, and other ocular disorders.
9. Cetuximab (Erbitux): A chimeric monoclonal antibody that binds to epidermal growth factor receptor (EGFR), used in the treatment of colorectal cancer and head and neck squamous cell carcinoma.
10. Adalimumab (Humira): A fully humanized monoclonal antibody that targets tumor necrosis factor-alpha (TNF-α), used in the treatment of various inflammatory diseases, including rheumatoid arthritis, psoriasis, and Crohn's disease.
11. Bevacizumab (Avastin): A recombinant humanized monoclonal antibody that binds to VEGF-A, used in the treatment of various cancers, including colorectal, lung, breast, and kidney cancer.
12. Trastuzumab (Herceptin): A humanized monoclonal antibody that targets HER2/neu receptor, used in the treatment of breast cancer.
13. Rituximab (Rituxan): A chimeric monoclonal antibody that binds to CD20 antigen on B cells, used in the treatment of non-Hodgkin's lymphoma and rheumatoid arthritis.
14. Palivizumab (Synagis): A humanized monoclonal antibody that binds to the F protein of respiratory syncytial virus, used in the prevention of respiratory syncytial virus infection in high-risk infants.
15. Infliximab (Remicade): A chimeric monoclonal antibody that targets TNF-α, used in the treatment of various inflammatory diseases, including Crohn's disease, ulcerative colitis, rheumatoid arthritis, and ankylosing spondylitis.
16. Natalizumab (Tysabri): A humanized monoclonal antibody that binds to α4β1 integrin, used in the treatment of multiple sclerosis and Crohn's disease.
17. Adalimumab (Humira): A fully human monoclonal antibody that targets TNF-α, used in the treatment of various inflammatory diseases, including rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, Crohn's disease, and ulcerative colitis.
18. Golimumab (Simponi): A fully human monoclonal antibody that targets TNF-α, used in the treatment of rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and ulcerative colitis.
19. Certolizumab pegol (Cimzia): A PEGylated Fab' fragment of a humanized monoclonal antibody that targets TNF-α, used in the treatment of rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and Crohn's disease.
20. Ustekinumab (Stelara): A fully human monoclonal antibody that targets IL-12 and IL-23, used in the treatment of psoriasis, psoriatic arthritis, and Crohn's disease.
21. Secukinumab (Cosentyx): A fully human monoclonal antibody that targets IL-17A, used in the treatment of psoriasis, psoriatic arthritis, and ankylosing spondylitis.
22. Ixekizumab (Taltz): A fully human monoclonal antibody that targets IL-17A, used in the treatment of psoriasis and psoriatic arthritis.
23. Brodalumab (Siliq): A fully human monoclonal antibody that targets IL-17 receptor A, used in the treatment of psoriasis.
24. Sarilumab (Kevzara): A fully human monoclonal antibody that targets the IL-6 receptor, used in the treatment of rheumatoid arthritis.
25. Tocilizumab (Actemra): A humanized monoclonal antibody that targets the IL-6 receptor, used in the treatment of rheumatoid arthritis, systemic juvenile idiopathic arthritis, polyarticular juvenile idiopathic arthritis, giant cell arteritis, and chimeric antigen receptor T-cell-induced cytokine release syndrome.
26. Siltuximab (Sylvant): A chimeric monoclonal antibody that targets IL-6, used in the treatment of multicentric Castleman disease.
27. Satralizumab (Enspryng): A humanized monoclonal antibody that targets IL-6 receptor alpha, used in the treatment of neuromyelitis optica spectrum disorder.
28. Sirukumab (Plivensia): A human monoclonal antibody that targets IL-6, used in the treatment

Carrier proteins, also known as transport proteins, are a type of protein that facilitates the movement of molecules across cell membranes. They are responsible for the selective and active transport of ions, sugars, amino acids, and other molecules from one side of the membrane to the other, against their concentration gradient. This process requires energy, usually in the form of ATP (adenosine triphosphate).

Carrier proteins have a specific binding site for the molecule they transport, and undergo conformational changes upon binding, which allows them to move the molecule across the membrane. Once the molecule has been transported, the carrier protein returns to its original conformation, ready to bind and transport another molecule.

Carrier proteins play a crucial role in maintaining the balance of ions and other molecules inside and outside of cells, and are essential for many physiological processes, including nerve impulse transmission, muscle contraction, and nutrient uptake.

Virus replication is the process by which a virus produces copies or reproduces itself inside a host cell. This involves several steps:

1. Attachment: The virus attaches to a specific receptor on the surface of the host cell.
2. Penetration: The viral genetic material enters the host cell, either by invagination of the cell membrane or endocytosis.
3. Uncoating: The viral genetic material is released from its protective coat (capsid) inside the host cell.
4. Replication: The viral genetic material uses the host cell's machinery to produce new viral components, such as proteins and nucleic acids.
5. Assembly: The newly synthesized viral components are assembled into new virus particles.
6. Release: The newly formed viruses are released from the host cell, often through lysis (breaking) of the cell membrane or by budding off the cell membrane.

The specific mechanisms and details of virus replication can vary depending on the type of virus. Some viruses, such as DNA viruses, use the host cell's DNA polymerase to replicate their genetic material, while others, such as RNA viruses, use their own RNA-dependent RNA polymerase or reverse transcriptase enzymes. Understanding the process of virus replication is important for developing antiviral therapies and vaccines.

Tumor suppressor protein p53, also known as p53 or tumor protein p53, is a nuclear phosphoprotein that plays a crucial role in preventing cancer development and maintaining genomic stability. It does so by regulating the cell cycle and acting as a transcription factor for various genes involved in apoptosis (programmed cell death), DNA repair, and cell senescence (permanent cell growth arrest).

In response to cellular stress, such as DNA damage or oncogene activation, p53 becomes activated and accumulates in the nucleus. Activated p53 can then bind to specific DNA sequences and promote the transcription of target genes that help prevent the proliferation of potentially cancerous cells. These targets include genes involved in cell cycle arrest (e.g., CDKN1A/p21), apoptosis (e.g., BAX, PUMA), and DNA repair (e.g., GADD45).

Mutations in the TP53 gene, which encodes p53, are among the most common genetic alterations found in human cancers. These mutations often lead to a loss or reduction of p53's tumor suppressive functions, allowing cancer cells to proliferate uncontrollably and evade apoptosis. As a result, p53 has been referred to as "the guardian of the genome" due to its essential role in preventing tumorigenesis.

Protein isoforms are different forms or variants of a protein that are produced from a single gene through the process of alternative splicing, where different exons (or parts of exons) are included in the mature mRNA molecule. This results in the production of multiple, slightly different proteins that share a common core structure but have distinct sequences and functions. Protein isoforms can also arise from genetic variations such as single nucleotide polymorphisms or mutations that alter the protein-coding sequence of a gene. These differences in protein sequence can affect the stability, localization, activity, or interaction partners of the protein isoform, leading to functional diversity and specialization within cells and organisms.

Immediate-early proteins (IEPs) are a class of regulatory proteins that play a crucial role in the early stages of gene expression in viral infection and cellular stress responses. These proteins are synthesized rapidly, without the need for new protein synthesis, after the induction of immediate-early genes (IEGs).

In the context of viral infection, IEPs are often the first proteins produced by the virus upon entry into the host cell. They function as transcription factors that bind to specific DNA sequences and regulate the expression of early and late viral genes required for replication and packaging of the viral genome.

IEPs can also be involved in modulating host cell signaling pathways, altering cell cycle progression, and inducing apoptosis (programmed cell death). Dysregulation of IEPs has been implicated in various diseases, including cancer and neurological disorders.

It is important to note that the term "immediate-early proteins" is primarily used in the context of viral infection, while in other contexts such as cellular stress responses or oncogene activation, these proteins may be referred to by different names, such as "early response genes" or "transcription factors."

Small interfering RNA (siRNA) is a type of short, double-stranded RNA molecule that plays a role in the RNA interference (RNAi) pathway. The RNAi pathway is a natural cellular process that regulates gene expression by targeting and destroying specific messenger RNA (mRNA) molecules, thereby preventing the translation of those mRNAs into proteins.

SiRNAs are typically 20-25 base pairs in length and are generated from longer double-stranded RNA precursors called hairpin RNAs or dsRNAs by an enzyme called Dicer. Once generated, siRNAs associate with a protein complex called the RNA-induced silencing complex (RISC), which uses one strand of the siRNA (the guide strand) to recognize and bind to complementary sequences in the target mRNA. The RISC then cleaves the target mRNA, leading to its degradation and the inhibition of protein synthesis.

SiRNAs have emerged as a powerful tool for studying gene function and have shown promise as therapeutic agents for a variety of diseases, including viral infections, cancer, and genetic disorders. However, their use as therapeutics is still in the early stages of development, and there are challenges associated with delivering siRNAs to specific cells and tissues in the body.

COS cells are a type of cell line that are commonly used in molecular biology and genetic research. The name "COS" is an acronym for "CV-1 in Origin," as these cells were originally derived from the African green monkey kidney cell line CV-1. COS cells have been modified through genetic engineering to express high levels of a protein called SV40 large T antigen, which allows them to efficiently take up and replicate exogenous DNA.

There are several different types of COS cells that are commonly used in research, including COS-1, COS-3, and COS-7 cells. These cells are widely used for the production of recombinant proteins, as well as for studies of gene expression, protein localization, and signal transduction.

It is important to note that while COS cells have been a valuable tool in scientific research, they are not without their limitations. For example, because they are derived from monkey kidney cells, there may be differences in the way that human genes are expressed or regulated in these cells compared to human cells. Additionally, because COS cells express SV40 large T antigen, they may have altered cell cycle regulation and other phenotypic changes that could affect experimental results. Therefore, it is important to carefully consider the choice of cell line when designing experiments and interpreting results.

RNA interference (RNAi) is a biological process in which RNA molecules inhibit the expression of specific genes. This process is mediated by small RNA molecules, including microRNAs (miRNAs) and small interfering RNAs (siRNAs), that bind to complementary sequences on messenger RNA (mRNA) molecules, leading to their degradation or translation inhibition.

RNAi plays a crucial role in regulating gene expression and defending against foreign genetic elements, such as viruses and transposons. It has also emerged as an important tool for studying gene function and developing therapeutic strategies for various diseases, including cancer and viral infections.

Adaptor proteins are a type of protein that play a crucial role in intracellular signaling pathways by serving as a link between different components of the signaling complex. Specifically, "signal transducing adaptor proteins" refer to those adaptor proteins that are involved in signal transduction processes, where they help to transmit signals from the cell surface receptors to various intracellular effectors. These proteins typically contain modular domains that allow them to interact with multiple partners, thereby facilitating the formation of large signaling complexes and enabling the integration of signals from different pathways.

Signal transducing adaptor proteins can be classified into several families based on their structural features, including the Src homology 2 (SH2) domain, the Src homology 3 (SH3) domain, and the phosphotyrosine-binding (PTB) domain. These domains enable the adaptor proteins to recognize and bind to specific motifs on other signaling molecules, such as receptor tyrosine kinases, G protein-coupled receptors, and cytokine receptors.

One well-known example of a signal transducing adaptor protein is the growth factor receptor-bound protein 2 (Grb2), which contains an SH2 domain that binds to phosphotyrosine residues on activated receptor tyrosine kinases. Grb2 also contains an SH3 domain that interacts with proline-rich motifs on other signaling proteins, such as the guanine nucleotide exchange factor SOS. This interaction facilitates the activation of the Ras small GTPase and downstream signaling pathways involved in cell growth, differentiation, and survival.

Overall, signal transducing adaptor proteins play a critical role in regulating various cellular processes by modulating intracellular signaling pathways in response to extracellular stimuli. Dysregulation of these proteins has been implicated in various diseases, including cancer and inflammatory disorders.

I'm sorry for any confusion, but "Leukemia P388" is not a widely recognized medical term or a specific type of leukemia. The term "P388" is often used to refer to a particular type of mouse leukemia that is commonly used in laboratory research for testing potential anti-cancer drugs.

Leukemia, in general, is a type of cancer that originates in the bone marrow and results in an overproduction of abnormal white blood cells (leukocytes). These abnormal cells crowd out the healthy cells in the bone marrow, leading to a weakened immune system and various complications.

There are many different types of leukemia, classified based on the type of white blood cell affected (myeloid or lymphocytic) and the speed of progression (acute or chronic). If you're looking for information about a specific type of leukemia, I would be happy to help if you could provide more details.

Biphenotypic acute leukemia (BAL) is a rare subtype of acute leukemia that possesses the features of both myeloid and lymphoid lineages. It is characterized by the presence of blasts that express antigens associated with both cell lines, which can make it challenging to diagnose and treat. BAL is considered an aggressive form of leukemia and requires prompt medical attention and treatment. The exact cause of BAL is not well understood, but like other forms of leukemia, it is thought to result from genetic mutations that lead to uncontrolled cell growth and division.

Molecular sequence data refers to the specific arrangement of molecules, most commonly nucleotides in DNA or RNA, or amino acids in proteins, that make up a biological macromolecule. This data is generated through laboratory techniques such as sequencing, and provides information about the exact order of the constituent molecules. This data is crucial in various fields of biology, including genetics, evolution, and molecular biology, allowing for comparisons between different organisms, identification of genetic variations, and studies of gene function and regulation.

A mutation is a permanent change in the DNA sequence of an organism's genome. Mutations can occur spontaneously or be caused by environmental factors such as exposure to radiation, chemicals, or viruses. They may have various effects on the organism, ranging from benign to harmful, depending on where they occur and whether they alter the function of essential proteins. In some cases, mutations can increase an individual's susceptibility to certain diseases or disorders, while in others, they may confer a survival advantage. Mutations are the driving force behind evolution, as they introduce new genetic variability into populations, which can then be acted upon by natural selection.

Intracellular signaling peptides and proteins are molecules that play a crucial role in transmitting signals within cells, which ultimately lead to changes in cell behavior or function. These signals can originate from outside the cell (extracellular) or within the cell itself. Intracellular signaling molecules include various types of peptides and proteins, such as:

1. G-protein coupled receptors (GPCRs): These are seven-transmembrane domain receptors that bind to extracellular signaling molecules like hormones, neurotransmitters, or chemokines. Upon activation, they initiate a cascade of intracellular signals through G proteins and secondary messengers.
2. Receptor tyrosine kinases (RTKs): These are transmembrane receptors that bind to growth factors, cytokines, or hormones. Activation of RTKs leads to autophosphorylation of specific tyrosine residues, creating binding sites for intracellular signaling proteins such as adapter proteins, phosphatases, and enzymes like Ras, PI3K, and Src family kinases.
3. Second messenger systems: Intracellular second messengers are small molecules that amplify and propagate signals within the cell. Examples include cyclic adenosine monophosphate (cAMP), cyclic guanosine monophosphate (cGMP), diacylglycerol (DAG), inositol triphosphate (IP3), calcium ions (Ca2+), and nitric oxide (NO). These second messengers activate or inhibit various downstream effectors, leading to changes in cellular responses.
4. Signal transduction cascades: Intracellular signaling proteins often form complex networks of interacting molecules that relay signals from the plasma membrane to the nucleus. These cascades involve kinases (protein kinases A, B, C, etc.), phosphatases, and adapter proteins, which ultimately regulate gene expression, cell cycle progression, metabolism, and other cellular processes.
5. Ubiquitination and proteasome degradation: Intracellular signaling pathways can also control protein stability by modulating ubiquitin-proteasome degradation. E3 ubiquitin ligases recognize specific substrates and conjugate them with ubiquitin molecules, targeting them for proteasomal degradation. This process regulates the abundance of key signaling proteins and contributes to signal termination or amplification.

In summary, intracellular signaling pathways involve a complex network of interacting proteins that relay signals from the plasma membrane to various cellular compartments, ultimately regulating gene expression, metabolism, and other cellular processes. Dysregulation of these pathways can contribute to disease development and progression, making them attractive targets for therapeutic intervention.

Fibroblasts are specialized cells that play a critical role in the body's immune response and wound healing process. They are responsible for producing and maintaining the extracellular matrix (ECM), which is the non-cellular component present within all tissues and organs, providing structural support and biochemical signals for surrounding cells.

Fibroblasts produce various ECM proteins such as collagens, elastin, fibronectin, and laminins, forming a complex network of fibers that give tissues their strength and flexibility. They also help in the regulation of tissue homeostasis by controlling the turnover of ECM components through the process of remodeling.

In response to injury or infection, fibroblasts become activated and start to proliferate rapidly, migrating towards the site of damage. Here, they participate in the inflammatory response, releasing cytokines and chemokines that attract immune cells to the area. Additionally, they deposit new ECM components to help repair the damaged tissue and restore its functionality.

Dysregulation of fibroblast activity has been implicated in several pathological conditions, including fibrosis (excessive scarring), cancer (where they can contribute to tumor growth and progression), and autoimmune diseases (such as rheumatoid arthritis).

Friend murine leukemia virus (F-MuLV) is a type of retrovirus that specifically infects mice. It was first discovered by Charlotte Friend in the 1950s and has since been widely used as a model system to study retroviral pathogenesis, oncogenesis, and immune responses.

F-MuLV is a complex retrovirus that contains several accessory genes, including gag, pol, env, and others. The virus can cause leukemia and other malignancies in susceptible mice, particularly when it is transmitted from mother to offspring through the milk.

The virus is also known to induce immunosuppression, which makes infected mice more susceptible to other infections and diseases. F-MuLV has been used extensively in laboratory research to investigate various aspects of retroviral biology, including viral entry, replication, gene expression, and host immune responses.

It is important to note that Friend murine leukemia virus only infects mice and is not known to cause any disease in humans or other animals.

Western blotting is a laboratory technique used in molecular biology to detect and quantify specific proteins in a mixture of many different proteins. This technique is commonly used to confirm the expression of a protein of interest, determine its size, and investigate its post-translational modifications. The name "Western" blotting distinguishes this technique from Southern blotting (for DNA) and Northern blotting (for RNA).

The Western blotting procedure involves several steps:

1. Protein extraction: The sample containing the proteins of interest is first extracted, often by breaking open cells or tissues and using a buffer to extract the proteins.
2. Separation of proteins by electrophoresis: The extracted proteins are then separated based on their size by loading them onto a polyacrylamide gel and running an electric current through the gel (a process called sodium dodecyl sulfate-polyacrylamide gel electrophoresis or SDS-PAGE). This separates the proteins according to their molecular weight, with smaller proteins migrating faster than larger ones.
3. Transfer of proteins to a membrane: After separation, the proteins are transferred from the gel onto a nitrocellulose or polyvinylidene fluoride (PVDF) membrane using an electric current in a process called blotting. This creates a replica of the protein pattern on the gel but now immobilized on the membrane for further analysis.
4. Blocking: The membrane is then blocked with a blocking agent, such as non-fat dry milk or bovine serum albumin (BSA), to prevent non-specific binding of antibodies in subsequent steps.
5. Primary antibody incubation: A primary antibody that specifically recognizes the protein of interest is added and allowed to bind to its target protein on the membrane. This step may be performed at room temperature or 4°C overnight, depending on the antibody's properties.
6. Washing: The membrane is washed with a buffer to remove unbound primary antibodies.
7. Secondary antibody incubation: A secondary antibody that recognizes the primary antibody (often coupled to an enzyme or fluorophore) is added and allowed to bind to the primary antibody. This step may involve using a horseradish peroxidase (HRP)-conjugated or alkaline phosphatase (AP)-conjugated secondary antibody, depending on the detection method used later.
8. Washing: The membrane is washed again to remove unbound secondary antibodies.
9. Detection: A detection reagent is added to visualize the protein of interest by detecting the signal generated from the enzyme-conjugated or fluorophore-conjugated secondary antibody. This can be done using chemiluminescent, colorimetric, or fluorescent methods.
10. Analysis: The resulting image is analyzed to determine the presence and quantity of the protein of interest in the sample.

Western blotting is a powerful technique for identifying and quantifying specific proteins within complex mixtures. It can be used to study protein expression, post-translational modifications, protein-protein interactions, and more. However, it requires careful optimization and validation to ensure accurate and reproducible results.

Repressor proteins are a type of regulatory protein in molecular biology that suppress the transcription of specific genes into messenger RNA (mRNA) by binding to DNA. They function as part of gene regulation processes, often working in conjunction with an operator region and a promoter region within the DNA molecule. Repressor proteins can be activated or deactivated by various signals, allowing for precise control over gene expression in response to changing cellular conditions.

There are two main types of repressor proteins:

1. DNA-binding repressors: These directly bind to specific DNA sequences (operator regions) near the target gene and prevent RNA polymerase from transcribing the gene into mRNA.
2. Allosteric repressors: These bind to effector molecules, which then cause a conformational change in the repressor protein, enabling it to bind to DNA and inhibit transcription.

Repressor proteins play crucial roles in various biological processes, such as development, metabolism, and stress response, by controlling gene expression patterns in cells.

Viral proteins are the proteins that are encoded by the viral genome and are essential for the viral life cycle. These proteins can be structural or non-structural and play various roles in the virus's replication, infection, and assembly process. Structural proteins make up the physical structure of the virus, including the capsid (the protein shell that surrounds the viral genome) and any envelope proteins (that may be present on enveloped viruses). Non-structural proteins are involved in the replication of the viral genome and modulation of the host cell environment to favor viral replication. Overall, a thorough understanding of viral proteins is crucial for developing antiviral therapies and vaccines.

HL-60 cells are a type of human promyelocytic leukemia cell line that is commonly used in scientific research. They are named after the hospital where they were first isolated, the Hospital of the University of Pennsylvania (HUP) and the 60th culture attempt to grow these cells.

HL-60 cells have the ability to differentiate into various types of blood cells, such as granulocytes, monocytes, and macrophages, when exposed to certain chemical compounds or under specific culturing conditions. This makes them a valuable tool for studying the mechanisms of cell differentiation, proliferation, and apoptosis (programmed cell death).

HL-60 cells are also often used in toxicity studies, drug discovery and development, and research on cancer, inflammation, and infectious diseases. They can be easily grown in the lab and have a stable genotype, making them ideal for use in standardized experiments and comparisons between different studies.

Protein transport, in the context of cellular biology, refers to the process by which proteins are actively moved from one location to another within or between cells. This is a crucial mechanism for maintaining proper cell function and regulation.

Intracellular protein transport involves the movement of proteins within a single cell. Proteins can be transported across membranes (such as the nuclear envelope, endoplasmic reticulum, Golgi apparatus, or plasma membrane) via specialized transport systems like vesicles and transport channels.

Intercellular protein transport refers to the movement of proteins from one cell to another, often facilitated by exocytosis (release of proteins in vesicles) and endocytosis (uptake of extracellular substances via membrane-bound vesicles). This is essential for communication between cells, immune response, and other physiological processes.

It's important to note that any disruption in protein transport can lead to various diseases, including neurological disorders, cancer, and metabolic conditions.

Adult T-cell Leukemia/Lymphoma (ATLL) is a rare and aggressive type of cancer that affects the circulating white blood cells called T-lymphocytes or T-cells. It is caused by the human T-cell leukemia virus type 1 (HTLV-1), which infects CD4+ T-cells and leads to their malignant transformation. The disease can present as either acute or chronic leukemia, or as lymphoma, depending on the clinical features and laboratory findings.

The acute form of ATLL is characterized by the rapid proliferation of abnormal T-cells in the blood, bone marrow, and other organs. Patients with acute ATLL typically have a poor prognosis, with a median survival of only a few months. Symptoms may include skin rashes, lymphadenopathy (swollen lymph nodes), hepatosplenomegaly (enlarged liver and spleen), and hypercalcemia (high levels of calcium in the blood).

The chronic form of ATLL is less aggressive than the acute form, but it can still lead to serious complications. Chronic ATLL is characterized by the accumulation of abnormal T-cells in the blood and lymph nodes, as well as skin lesions and hypercalcemia. The median survival for patients with chronic ATLL is around two years.

ATLL can also present as a lymphoma, which is characterized by the proliferation of abnormal T-cells in the lymph nodes, spleen, and other organs. Lymphoma may occur in isolation or in combination with leukemic features.

The diagnosis of ATLL is based on clinical findings, laboratory tests, and the detection of HTLV-1 antibodies or proviral DNA in the blood or tissue samples. Treatment options for ATLL include chemotherapy, antiretroviral therapy, immunotherapy, and stem cell transplantation. The choice of treatment depends on several factors, including the patient's age, overall health, and the stage and type of ATLL.

Cytarabine is a chemotherapeutic agent used in the treatment of various types of cancer, including leukemias and lymphomas. Its chemical name is cytosine arabinoside, and it works by interfering with the DNA synthesis of cancer cells, which ultimately leads to their death.

Cytarabine is often used in combination with other chemotherapy drugs and may be administered through various routes, such as intravenous (IV) or subcutaneous injection, or orally. The specific dosage and duration of treatment will depend on the type and stage of cancer being treated, as well as the patient's overall health status.

Like all chemotherapy drugs, cytarabine can cause a range of side effects, including nausea, vomiting, diarrhea, hair loss, and an increased risk of infection. It may also cause more serious side effects, such as damage to the liver, kidneys, or nervous system, and it is important for patients to be closely monitored during treatment to minimize these risks.

It's important to note that medical treatments should only be administered under the supervision of a qualified healthcare professional, and this information should not be used as a substitute for medical advice.

An amino acid sequence is the specific order of amino acids in a protein or peptide molecule, formed by the linking of the amino group (-NH2) of one amino acid to the carboxyl group (-COOH) of another amino acid through a peptide bond. The sequence is determined by the genetic code and is unique to each type of protein or peptide. It plays a crucial role in determining the three-dimensional structure and function of proteins.

Acute Megakaryoblastic Leukemia (AMKL) is a type of cancer that affects the blood and bone marrow. Specifically, it is a subtype of acute myeloid leukemia (AML), which is characterized by the rapid growth of abnormal cells in the bone marrow that interfere with the production of normal blood cells.

In AMKL, the abnormal cells are megakaryoblasts, which are immature cells that should develop into platelet-producing cells called megakaryocytes. However, in AMKL, these cells do not mature properly and instead accumulate in the bone marrow and bloodstream, leading to a shortage of healthy blood cells.

Symptoms of AMKL may include fatigue, weakness, frequent infections, easy bruising or bleeding, and the appearance of small red spots on the skin (petechiae). Diagnosis typically involves a combination of physical exam, medical history, blood tests, bone marrow aspiration and biopsy, and sometimes imaging studies.

Treatment for AMKL usually involves a combination of chemotherapy, radiation therapy, and/or stem cell transplantation. The specific treatment plan will depend on several factors, including the patient's age, overall health, and the extent of the disease.

The AKR murine leukemia virus (AKR MLV) is a type of retrovirus that naturally infects mice of the AKR strain. It is a member of the gammaretrovirus genus and is closely related to other murine leukemia viruses (MLVs).

AKR MLV is transmitted horizontally through close contact with infected animals, as well as vertically from mother to offspring. The virus primarily infects hematopoietic cells, including lymphocytes and macrophages, and can cause a variety of diseases, most notably leukemia and lymphoma.

The AKR MLV genome contains three main structural genes: gag, pol, and env, which encode the viral matrix, capsid, nucleocapsid, reverse transcriptase, integrase, and envelope proteins, respectively. Additionally, the virus carries accessory genes, such as rex and sor, that play a role in regulating viral gene expression and replication.

AKR MLV has been extensively studied as a model system for retrovirus biology and pathogenesis, and its study has contributed significantly to our understanding of the mechanisms of retroviral infection, replication, and disease.

A fusion protein known as "BCR-ABL" is formed due to a genetic abnormality called the Philadelphia chromosome (derived from a reciprocal translocation between chromosomes 9 and 22). This results in the formation of the oncogenic BCR-ABL tyrosine kinase, which contributes to unregulated cell growth and division, leading to chronic myeloid leukemia (CML) and some types of acute lymphoblastic leukemia (ALL). The BCR-ABL fusion protein has constitutively active tyrosine kinase activity, which results in the activation of various signaling pathways promoting cell proliferation, survival, and inhibition of apoptosis. This genetic alteration is crucial in the development and progression of CML and some types of ALL, making BCR-ABL an important therapeutic target for these malignancies.

"Cells, cultured" is a medical term that refers to cells that have been removed from an organism and grown in controlled laboratory conditions outside of the body. This process is called cell culture and it allows scientists to study cells in a more controlled and accessible environment than they would have inside the body. Cultured cells can be derived from a variety of sources, including tissues, organs, or fluids from humans, animals, or cell lines that have been previously established in the laboratory.

Cell culture involves several steps, including isolation of the cells from the tissue, purification and characterization of the cells, and maintenance of the cells in appropriate growth conditions. The cells are typically grown in specialized media that contain nutrients, growth factors, and other components necessary for their survival and proliferation. Cultured cells can be used for a variety of purposes, including basic research, drug development and testing, and production of biological products such as vaccines and gene therapies.

It is important to note that cultured cells may behave differently than they do in the body, and results obtained from cell culture studies may not always translate directly to human physiology or disease. Therefore, it is essential to validate findings from cell culture experiments using additional models and ultimately in clinical trials involving human subjects.

Chronic myeloid leukemia (CML) is a type of cancer that starts in certain blood-forming cells of the bone marrow. In chronic phase CML, the disease progresses slowly and may not cause any symptoms for a period of time. It is characterized by the overproduction of mature and immature white blood cells, called myeloid cells. These cells accumulate in the bone marrow and interfere with the production of normal blood cells, leading to anemia, fatigue, easy bruising, and increased risk of infection. The distinguishing genetic feature of CML is the presence of the Philadelphia chromosome, which is formed by a genetic translocation between chromosomes 9 and 22, resulting in the formation of the BCR-ABL fusion gene. This gene produces an abnormal protein that contributes to the development of leukemia. The chronic phase of CML can last for several years and is typically treated with targeted therapy such as tyrosine kinase inhibitors (TKIs) which target the BCR-ABL protein.

Precursor B-cell Acute Lymphoblastic Leukemia/Lymphoma (also known as Precursor B-cell ALL or Precursor B-cell Non-Hodgkin Lymphoma) is a type of cancer that affects the early stages of B-cell development. It is characterized by the uncontrolled proliferation of immature B-cells, also known as lymphoblasts, in the bone marrow, blood, and sometimes in other organs such as the lymph nodes. These malignant cells accumulate and interfere with the normal production of blood cells, leading to symptoms such as anemia, infection, and bleeding.

The distinction between Precursor B-cell ALL and Precursor B-cell Lymphoma is based on the site of involvement. If the majority of the cancerous cells are found in the bone marrow and/or blood, it is classified as a leukemia (ALL). However, if the malignant cells primarily involve the lymph nodes or other extramedullary sites, it is considered a lymphoma. Despite this distinction, both entities share similar biological features, treatment approaches, and prognoses.

It's important to note that medical definitions can vary slightly based on the source and context. For the most accurate information, consult authoritative resources such as medical textbooks or peer-reviewed articles.

Antineoplastic agents are a class of drugs used to treat malignant neoplasms or cancer. These agents work by inhibiting the growth and proliferation of cancer cells, either by killing them or preventing their division and replication. Antineoplastic agents can be classified based on their mechanism of action, such as alkylating agents, antimetabolites, topoisomerase inhibitors, mitotic inhibitors, and targeted therapy agents.

Alkylating agents work by adding alkyl groups to DNA, which can cause cross-linking of DNA strands and ultimately lead to cell death. Antimetabolites interfere with the metabolic processes necessary for DNA synthesis and replication, while topoisomerase inhibitors prevent the relaxation of supercoiled DNA during replication. Mitotic inhibitors disrupt the normal functioning of the mitotic spindle, which is essential for cell division. Targeted therapy agents are designed to target specific molecular abnormalities in cancer cells, such as mutated oncogenes or dysregulated signaling pathways.

It's important to note that antineoplastic agents can also affect normal cells and tissues, leading to various side effects such as nausea, vomiting, hair loss, and myelosuppression (suppression of bone marrow function). Therefore, the use of these drugs requires careful monitoring and management of their potential adverse effects.

Daunorubicin is an anthracycline antibiotic used in the treatment of various types of cancer, including leukemia, Hodgkin's lymphoma, and breast cancer. It works by intercalating with DNA and inhibiting topoisomerase II, which results in DNA damage and ultimately cell death.

The drug is administered intravenously and may cause side effects such as nausea, vomiting, hair loss, mouth sores, and damage to the heart muscle (cardiotoxicity) with long-term use. Regular monitoring of cardiac function is recommended during treatment with daunorubicin.

It's important to note that this medication should only be used under the supervision of a qualified healthcare professional, as it can have serious and potentially life-threatening consequences if not used correctly.

Plasma cell leukemia (PCL) is a rare and aggressive type of cancer that involves the uncontrolled multiplication of malignant plasma cells in the bone marrow, blood, and sometimes in other organs. Plasma cells are a type of white blood cell that produces antibodies to help fight infections. In PCL, the malignant plasma cells produce abnormal antibodies called M-proteins or paraproteins, which can accumulate in various tissues and cause damage.

PCL is typically classified into two types: primary and secondary. Primary PCL is a distinct clinical entity that presents with more than 20% plasma cells in the bone marrow and/or blood. Secondary PCL is a complication of multiple myeloma, a more common type of plasma cell cancer, and occurs when the malignant plasma cells spread from the bone marrow to the blood.

The symptoms of PCL are similar to those of other types of leukemia and may include fatigue, weakness, weight loss, frequent infections, easy bruising or bleeding, and bone pain. Diagnosis of PCL typically involves a combination of clinical evaluation, laboratory tests, imaging studies, and bone marrow aspiration and biopsy. Treatment options for PCL may include chemotherapy, stem cell transplantation, radiation therapy, and targeted therapies. The prognosis for patients with PCL is generally poor, with a median survival time of less than one year.

Accelerated Phase Leukemia, Myeloid is a stage in the progression of certain myeloid malignancies such as Chronic Myelogenous Leukemia (CML) or Myelodysplastic Syndromes (MDS). During this phase, there is an increase in the number of immature blood cells (blasts) in the bone marrow and/or blood compared to the chronic phase. However, it has not yet reached the level of blast proliferation seen in the blast crisis phase.

The accelerated phase is characterized by various laboratory and clinical features, including:
- A significant increase in the percentage of blasts (10-19%) in the peripheral blood or bone marrow
- An increase in the white blood cell count, typically over 50 x 10^9/L
- The presence of new cytogenetic abnormalities or an increasing number of existing chromosomal changes
- A decrease in platelet count and/or hemoglobin levels
- Increasing symptoms related to bone marrow failure, such as fatigue, infection, and bleeding

The accelerated phase often precedes the blast crisis phase, which is associated with a worse prognosis. Early detection and intervention in the accelerated phase may help improve treatment outcomes and delay progression to blast crisis.

Karyotyping is a medical laboratory test used to study the chromosomes in a cell. It involves obtaining a sample of cells from a patient, usually from blood or bone marrow, and then staining the chromosomes so they can be easily seen under a microscope. The chromosomes are then arranged in pairs based on their size, shape, and other features to create a karyotype. This visual representation allows for the identification and analysis of any chromosomal abnormalities, such as extra or missing chromosomes, or structural changes like translocations or inversions. These abnormalities can provide important information about genetic disorders, diseases, and developmental problems.

K562 cells are a type of human cancer cell that are commonly used in scientific research. They are derived from a patient with chronic myelogenous leukemia (CML), a type of cancer that affects the blood and bone marrow.

K562 cells are often used as a model system to study various biological processes, including cell signaling, gene expression, differentiation, and apoptosis (programmed cell death). They are also commonly used in drug discovery and development, as they can be used to test the effectiveness of potential new therapies against cancer.

K562 cells have several characteristics that make them useful for research purposes. They are easy to grow and maintain in culture, and they can be manipulated genetically to express or knock down specific genes. Additionally, K562 cells are capable of differentiating into various cell types, such as red blood cells and megakaryocytes, which allows researchers to study the mechanisms of cell differentiation.

It's important to note that while K562 cells are a valuable tool for research, they do not fully recapitulate the complexity of human CML or other cancers. Therefore, findings from studies using K562 cells should be validated in more complex model systems or in clinical trials before they can be translated into treatments for patients.

T-cell prolymphocytic leukemia (T-PLL) is a rare and aggressive type of leukemia, which is a cancer that affects the blood and bone marrow. Specifically, T-PLL arises from mature T-cells, a type of white blood cell that plays a crucial role in the body's immune response.

In T-PLL, there is an accumulation of abnormal prolymphocytes, a particular stage of T-cell development, in the peripheral blood, bone marrow, and sometimes lymph nodes and spleen. These malignant cells can crowd out healthy cells, leading to impaired immune function, anemia, and increased susceptibility to infections.

T-PLL is primarily a disease of older adults, with a median age at diagnosis around 65 years. It has a poor prognosis, with a median survival of less than two years, although treatment advances have improved outcomes for some patients. Treatment typically involves chemotherapy and/or stem cell transplantation.

Human T-lymphotropic virus 1 (HTLV-1) is a complex retrovirus that infects CD4+ T lymphocytes and can cause adult T-cell leukemia/lymphoma (ATLL) and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). The virus is primarily transmitted through breastfeeding, sexual contact, or contaminated blood products. After infection, the virus integrates into the host's genome and can remain latent for years or even decades before leading to disease. HTLV-1 is endemic in certain regions of the world, including Japan, the Caribbean, Central and South America, and parts of Africa.

Prolymphocytic leukemia (PLL) is a rare and aggressive type of chronic leukemia, characterized by the abnormal accumulation of prolymphocytes, a specific type of mature but immature lymphocyte, in the blood, bone marrow, and sometimes in other organs. There are two types of PLL: B-cell prolymphocytic leukemia (B-PLL) and T-cell prolymphocytic leukemia (T-PLL).

B-PLL is a very rare subtype of chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL), accounting for less than 1% of all leukemias. It primarily affects older adults, with a median age at diagnosis of around 60-70 years. The disease is characterized by the proliferation of malignant B-lymphocytes, known as prolymphocytes, which accumulate in the blood, bone marrow, and sometimes in other organs such as the lymph nodes, spleen, and liver.

T-PLL is an even rarer subtype of leukemia, accounting for less than 1% of all leukemias. It primarily affects older adults, with a median age at diagnosis of around 65 years. T-PLL arises from mature T-lymphocytes, which accumulate in the blood, bone marrow, and sometimes in other organs such as the lymph nodes, spleen, and liver.

The symptoms of PLL can vary but often include fatigue, weight loss, frequent infections, swollen lymph nodes, and a high white blood cell count. The diagnosis of PLL typically involves a combination of clinical evaluation, laboratory tests, imaging studies, and bone marrow aspiration and biopsy. Treatment options for PLL may include chemotherapy, targeted therapy, immunotherapy, stem cell transplantation, or a combination of these approaches.

Core Binding Factor Alpha 2 Subunit, also known as CBF-A2 or CEBP-α, is a protein that forms a complex with other proteins to act as a transcription factor. Transcription factors are proteins that help regulate the expression of genes by binding to specific DNA sequences and controlling the rate of transcription of genetic information from DNA to RNA.

CBF-A2 is a member of the CCAAT/enhancer-binding protein (C/EBP) family of transcription factors, which are important in regulating various biological processes such as cell growth, development, and inflammation. CBF-A2 forms a heterodimer with Core Binding Factor Beta (CBF-β) to form the active transcription factor complex known as the core binding factor (CBF).

The CBF complex binds to the CCAAT box, a specific DNA sequence found in the promoter regions of many genes. By binding to this sequence, the CBF complex can either activate or repress the transcription of target genes, depending on the context and the presence of other regulatory factors.

Mutations in the gene encoding CBF-A2 have been associated with several human diseases, including acute myeloid leukemia (AML) and multiple myeloma. In AML, mutations in the CBF-A2 gene can lead to the formation of abnormal CBF complexes that disrupt normal gene expression patterns and contribute to the development of leukemia.

Juvenile Myelomonocytic Leukemia (JMML) is a rare and aggressive type of childhood leukemia, characterized by the overproduction of myeloid and monocytic white blood cells in the bone marrow. These cells accumulate in the bloodstream, leading to an increased risk of infection, anemia, and bleeding. JMML is different from other types of leukemia because it involves both the myeloid and monocytic cell lines, and it often affects younger children, typically those under 4 years old. The exact cause of JMML is not fully understood, but it has been linked to genetic mutations in certain genes, such as PTPN11, NRAS, KRAS, CBL, and NF1. Treatment for JMML usually involves a combination of chemotherapy, stem cell transplantation, and supportive care.

Precursor T-cell lymphoblastic leukemia-lymphoma (previously known as T-cell acute lymphoblastic leukemia/lymphoma or T-ALL) is a type of cancer that affects the early stages of T-cell development. It is characterized by the uncontrolled proliferation and accumulation of malignant precursor T-cell lymphoblasts in the bone marrow, blood, and sometimes in other organs such as the lymph nodes, spleen, and liver. These malignant cells can interfere with the normal functioning of the bone marrow and immune system, leading to symptoms like fatigue, frequent infections, and anemia. The distinction between precursor T-cell lymphoblastic leukemia and lymphoma is based on the extent of involvement of extramedullary sites (like lymph nodes) and the proportion of bone marrow involvement. Treatment typically involves intensive chemotherapy regimens, with possible additional treatments such as stem cell transplantation or targeted therapy depending on the individual case.

Acute basophilic leukemia (ABL) is a rare and aggressive subtype of acute myeloid leukemia (AML), a type of cancer that affects the blood and bone marrow. In ABL, the malignancy originates from the transformation of hematopoietic stem cells into abnormal blast cells, specifically basophils, in the bone marrow. These blasts proliferate rapidly and disrupt normal blood cell production, leading to a significant decrease in functional red and white blood cells and platelets.

The medical definition of acute basophilic leukemia is:

A malignant neoplasm of hematopoietic stem cells characterized by the uncontrolled proliferation and accumulation of immature basophils (basophilic blasts) in the bone marrow, blood, and occasionally other tissues. This rapidly progressing disorder is accompanied by a decline in the production of normal blood cells, resulting in symptoms such as anemia, fatigue, infection, easy bruising, and bleeding. The diagnosis of ABL typically involves bone marrow aspiration and biopsy, cytogenetic analysis, immunophenotyping, and molecular genetic testing to confirm the presence of leukemic blasts and identify specific genetic abnormalities that can inform prognosis and treatment decisions.

A base sequence in the context of molecular biology refers to the specific order of nucleotides in a DNA or RNA molecule. In DNA, these nucleotides are adenine (A), guanine (G), cytosine (C), and thymine (T). In RNA, uracil (U) takes the place of thymine. The base sequence contains genetic information that is transcribed into RNA and ultimately translated into proteins. It is the exact order of these bases that determines the genetic code and thus the function of the DNA or RNA molecule.

Leukemic infiltration is the abnormal spread and accumulation of malignant white blood cells (leukemia cells) in various tissues and organs outside the bone marrow. The bone marrow is the spongy tissue inside bones where blood cells are normally produced. In leukemia, the bone marrow produces large numbers of abnormal white blood cells that do not function properly. These abnormal cells can sometimes spill into the bloodstream and infiltrate other organs, such as the lymph nodes, spleen, liver, and central nervous system (brain and spinal cord). Leukemic infiltration can cause damage to these organs and lead to various symptoms. The pattern of organ involvement and the severity of infiltration depend on the type and stage of leukemia.

Asparaginase is a medication that is used in the treatment of certain types of cancer, such as acute lymphoblastic leukemia (ALL) and non-Hodgkin lymphoma (NHL). It is an enzyme that breaks down the amino acid asparagine, which is a building block of proteins. Some cancer cells are unable to produce their own asparagine and rely on obtaining it from the bloodstream. By reducing the amount of asparagine in the blood, asparaginase can help to slow or stop the growth of these cancer cells.

Asparaginase is usually given as an injection into a muscle (intramuscularly) or into a vein (intravenously). It may be given alone or in combination with other chemotherapy drugs. The specific dosage and duration of treatment will depend on the individual's medical history, the type and stage of cancer being treated, and how well the person tolerates the medication.

Like all medications, asparaginase can cause side effects. Common side effects include nausea, vomiting, loss of appetite, and changes in liver function tests. Less common but more serious side effects may include allergic reactions, pancreatitis, and blood clotting problems. It is important for patients to discuss the potential risks and benefits of asparaginase with their healthcare provider before starting treatment.

FMS-like tyrosine kinase 3 (FLT3) is a type of receptor tyrosine kinase, which is a type of enzyme that plays a role in signal transduction within cells. FLT3 is found on the surface of certain types of blood cells, including hematopoietic stem cells and some types of leukemia cells.

FLT3 is activated when it binds to its ligand, FLT3L, leading to activation of various signaling pathways that are involved in cell survival, proliferation, and differentiation. Mutations in the FLT3 gene can lead to constitutive activation of the receptor, even in the absence of its ligand, resulting in uncontrolled cell growth and division. Such mutations are commonly found in certain types of leukemia, including acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL), and are associated with a poor prognosis.

FLT3 inhibitors are a class of drugs that are being developed to target FLT3 mutations in leukemia cells, with the goal of blocking the abnormal signaling pathways that contribute to the growth and survival of these cancer cells.

The Philadelphia chromosome is a specific genetic alteration in certain types of leukemia and lymphoma, including chronic myelogenous leukemia (CML) and acute lymphoblastic leukemia (ALL). It is the result of a translocation between chromosomes 9 and 22, which forms an abnormal fusion gene called BCR-ABL. This gene produces an abnormal protein that leads to unregulated cell growth and division, causing cancer. The Philadelphia chromosome was first discovered in Philadelphia, USA, hence the name.

Lymphoma is a type of cancer that originates from the white blood cells called lymphocytes, which are part of the immune system. These cells are found in various parts of the body such as the lymph nodes, spleen, bone marrow, and other organs. Lymphoma can be classified into two main types: Hodgkin lymphoma (HL) and non-Hodgkin lymphoma (NHL).

HL is characterized by the presence of a specific type of abnormal lymphocyte called Reed-Sternberg cells, while NHL includes a diverse group of lymphomas that lack these cells. The symptoms of lymphoma may include swollen lymph nodes, fever, night sweats, weight loss, and fatigue.

The exact cause of lymphoma is not known, but it is believed to result from genetic mutations in the lymphocytes that lead to uncontrolled cell growth and division. Exposure to certain viruses, chemicals, and radiation may increase the risk of developing lymphoma. Treatment options for lymphoma depend on various factors such as the type and stage of the disease, age, and overall health of the patient. Common treatments include chemotherapy, radiation therapy, immunotherapy, and stem cell transplantation.

Chronic myeloid leukemia (CML), atypical, BCR-ABL negative is a rare subtype of CML that does not have the typical Philadelphia chromosome abnormality or the resulting BCR-ABL fusion gene. This means that the disease lacks the constitutively active tyrosine kinase that is targeted by imatinib mesylate (Gleevec) and other similar drugs.

The atypical form of CML is often characterized by a more aggressive clinical course, with a higher risk of transformation to acute leukemia compared to the classic form of CML. It can be difficult to diagnose and treat due to its rarity and heterogeneity. Treatment options may include chemotherapy, targeted therapy, stem cell transplantation, or a combination of these approaches. Regular follow-up with blood tests and bone marrow examinations is essential for monitoring the disease course and adjusting treatment as necessary.

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Tebar F, Bohlander SK, Sorkin A (1999). "Clathrin assembly lymphoid myeloid leukemia (CALM) protein: localization in endocytic- ... 2006). "Effect of clathrin assembly lymphoid myeloid leukemia protein depletion on clathrin coat formation". Traffic. 6 (12): ... "Clathrin assembly lymphoid myeloid leukemia (CALM) protein: localization in endocytic-coated pits, interactions with clathrin, ... 2007). "Acute myeloid leukemia is propagated by a leukemic stem cell with lymphoid characteristics in a mouse model of CALM/ ...
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MLL OMIM Entry: MYELOID/LYMPHOID OR MIXED LINEAGE LEUKEMIA GENE; MLL MLL+protein,+human at the U.S. National Library of ... myeloid/lymphoid or mixed-lineage leukemia 1 (MLL1), or zinc finger protein HRX (HRX), is an enzyme that in humans is encoded ... Multiple chromosomal translocations involving this gene are the cause of certain acute lymphoid leukemias and acute myeloid ... "Cooperativity in transcription factor binding to the coactivator CREB-binding protein (CBP). The mixed lineage leukemia protein ...
Myeloid/lymphoid or mixed-lineage leukemia 4, also known as MLL4, is a human gene. This gene encodes a protein which contains ... "Entrez Gene: MLL4 myeloid/lymphoid or mixed-lineage leukemia 4". Bedford MT, Chan DC, Leder P (1997). "FBP WW domains and the ... The SET domain is a conserved C-terminal domain that characterizes proteins of the MLL (mixed-lineage leukemia) family. This ... 2006). "A protein-protein interaction network for human inherited ataxias and disorders of Purkinje cell degeneration". Cell. ...
Tebar F, Bohlander SK, Sorkin A (1999). "Clathrin assembly lymphoid myeloid leukemia (CALM) protein: localization in endocytic- ... 2001). "Toward a catalog of human genes and proteins: sequencing and analysis of 500 novel complete protein coding human cDNAs ... AP-2 complex subunit alpha-1 is a protein that in humans is encoded by the AP2A1 gene. This gene encodes the alpha 1 adaptin ... Adaptor-related protein complex 2, alpha 1 has been shown to interact with DPYSL2 and NUMB. GRCh38: Ensembl release 89: ...
"Clathrin assembly lymphoid myeloid leukemia (CALM) protein: localization in endocytic-coated pits, interactions with clathrin, ... Clathrin heavy chain 1 is a protein that in humans is encoded by the CLTC gene. Clathrin is a major protein component of the ... 1999). "Paxillin LD4 motif binds PAK and PIX through a novel 95-kD ankyrin repeat, ARF-GAP protein: A role in cytoskeletal ... Murphy JE, Keen JH (1992). "Recognition sites for clathrin-associated proteins AP-2 and AP-3 on clathrin triskelia". J. Biol. ...
Tebar F, Bohlander SK, Sorkin A (August 1999). "Clathrin assembly lymphoid myeloid leukemia (CALM) protein: localization in ... Clathrin coat assembly protein AP180 is a protein that in humans is encoded by the SNAP91 gene. GRCh38: Ensembl release 89: ... X. The complete sequences of 100 new cDNA clones from brain which can code for large proteins in vitro". DNA Research. 5 (3): ... Yao PJ, Morsch R, Callahan LM, Coleman PD (1999). "Changes in synaptic expression of clathrin assembly protein AP180 in ...
... "myeloid/lymphoid or mixed-lineage leukemia (trithorax (Drosophila) homolog); translocated to, 2") and PBM1 ("pre-B-cell ... "brain protein I3 (BRI3)" (referring to the gene) and "brain protein I3 (BRI3)" (referring to the protein) are both valid. The ... It is also closely associated with protein nomenclature, as genes and the proteins they code for usually have similar ... The recommended formatting of printed gene and protein symbols varies between species. Vertebrate genes and proteins have names ...
"Entrez Gene: MLLT1 myeloid/lymphoid or mixed-lineage leukemia (trithorax homolog, Drosophila); translocated to, 1". García- ... encodes a nuclear protein with transcriptional activation potential in lymphoid and myeloid cells". Blood. 84 (6): 1747-52. doi ... leukemia". Leukemia. 21 (3): 588-90. doi:10.1038/sj.leu.2404542. PMID 17252016. MLLT1+protein,+human at the U.S. National ... "Retrovirus-mediated gene transfer of MLL-ELL transforms primary myeloid progenitors and causes acute myeloid leukemias in mice ...
... myeloid-lymphoid leukemia protein MeSH D12.776.624.664.700.167 - proto-oncogene proteins c-abl MeSH D12.776.624.664.700.168 - ... groel protein MeSH D12.776.602.500.500.100 - fusion proteins, bcr-abl MeSH D12.776.602.500.500.320 - fusion proteins, gag-onc ... oncogene protein v-maf MeSH D12.776.964.700.750.875 - oncogene proteins v-abl MeSH D12.776.964.700.750.882 - oncogene proteins ... fusion proteins, gag-pol MeSH D12.776.964.775.350.400 - hiv core protein p24 MeSH D12.776.964.775.375.325 - fusion proteins, ...
In fact, it's seen to complex with phosphatidylinositol clathrin assembly lymphoid-myeloid leukemia (PICALM), which would serve ... A family of proteins called muniscins are thought to be the primary allosteric activators of the AP2 adaptor complex, due to ... Henne WM, Boucrot E, Meinecke M, Evergren E, Vallis Y, Mittal R, McMahon HT (June 2010). "FCHo proteins are nucleators of ... The AP2 adaptor complex is a multimeric protein that works on the cell membrane to internalize cargo in clathrin-mediated ...
This gene is a member of the myeloid/lymphoid or mixed-lineage leukemia (MLL) family and encodes a protein with an N-terminal ... a homolog of Drosophila trithorax located within a segment of chromosome band 7q22 implicated in myeloid leukemia". Oncogene. ... Overexpression of the protein inhibits cell cycle progression. Alternate transcriptional splice variants have been ... Lysine methyltransferase 2E is a protein that in humans is encoded by the KMT2E gene. ...
Clathrin-assembly lymphoid myeloid leukaemia protein) is named after its association with myeloid and lymphoid leukemias where ... AP180 is a protein that plays an important role in clathrin-mediated endocytosis of synaptic vesicles. It is capable of ... In D. melanogaster it was also shown that AP180 is also required for either recycling vesicle proteins and/or maintaining the ... July 1999). "UNC-11, a Caenorhabditis elegans AP180 homologue, regulates the size and protein composition of synaptic vesicles ...
... of HOXA10 in murine hematopoietic cells perturbs both myeloid and lymphoid differentiation and leads to acute myeloid leukemia ... Homeobox protein Hox-A10 is a protein that in humans is encoded by the HOXA10 gene. In vertebrates, the genes encoding the ... induced differentiation of myeloid leukemia cell lines". The Journal of Biological Chemistry. 275 (26): 20117-26. doi:10.1074/ ... "AbdB-like Hox proteins stabilize DNA binding by the Meis1 homeodomain proteins". Molecular and Cellular Biology. 17 (11): 6448- ...
... a common MRV integration site in BXH2 myeloid leukemias, encodes a protein with homology to a lymphoid-restricted membrane ... a lymphoid-restricted protein whose expression is downregulated during myeloid differentiation. Therefore, this gene may be a ... Protein MRVI1 is a protein that in humans is encoded by the MRVI1 gene. This gene is similar to a mouse putative tumor ... myeloid leukemia tumor suppressor gene. Several alternatively spliced transcripts have been found for this gene, however, the ...
"Entrez Gene: MLLT4 myeloid/lymphoid or mixed-lineage leukemia (trithorax homolog, Drosophila); translocated to, 4". Radziwill G ... "Chimeric MLL products with a Ras binding cytoplasmic protein AF6 involved in t(6;11) (q27;q23) leukemia localize in the nucleus ... involved in acute myeloid leukemias with the t(6;11) chromosome translocation". Cancer Research. 53 (23): 5624-8. PMID 8242616 ... Afadin is a protein that in humans is encoded by the AFDN gene. Afadin is a Ras (see HRAS; MIM 190020) target that regulates ...
... clinical implications in myelodysplastic syndrome and acute lymphoid and myeloid leukemias". Leukemia. 19 (9): 1567-1572. doi: ... There is also a need to molecularly detect the presence of PML/RARA fusion protein, which is an oncogenic product of that ... "Acute Myeloid Leukemia Staging". Retrieved 26 August 2011. Mihova D. "Leukemia acute - Acute myeloid leukemia with minimal ... Acute myeloid leukemia (AML) is a cancer of the myeloid line of blood cells, characterized by the rapid growth of abnormal ...
... a consequence of chromosome translocations and are involved in the pathogenesis of myeloid/lymphoid or mixed lineage leukemia. ... The normal encoded protein is 1311 codons in length. It is expressed as an 8.7 kilobase transcript in the placenta and adult ... All AFF proteins are localized in the nucleus and have a role as transcriptional activators with a positive action on RNA ... AF4/FMR2 family member 2 is a protein that in humans is encoded by the AFF2 gene. Mutations in AFF2 are implicated in cases of ...
... in a lymphoid and t(9;15;12) in a myeloid leukemia". Blood. 90 (7): 2535-40. doi:10.1182/blood.V90.7.2535. PMID 9326218. TEL- ... "A TEL-JAK2 fusion protein with constitutive kinase activity in human leukemia". Science. 278 (5341): 1309-12. doi:10.1126/ ... The oligomerisation domain of the TEL protein (also called ETV6) becomes juxtaposed to the tyrosine kinase domain of JAK2, and ... TEL-JAK2 is a gene fusion resulting from a chromosomal translocation between chromosomes 9 and 12 observed in human leukemia. ...
... principally acute myeloid leukemia (AML), less commonly chronic myelomonocytic leukemia (CMML), and rarely a lymphoid leukemia ... located toward the proteins N-terminus) is responsible for interacting with various other nuclear proteins that regulate its ... GATA2 or GATA-binding factor 2 is a transcription factor, i.e. a nuclear protein which regulates the expression of genes. It ... Of its two zinc fingers, C-ZnF (located toward the protein's C-terminus) is responsible for binding to specific DNA sites while ...
... that involves this gene and the myeloid/lymphoid leukemia gene. Alternative splicing occurs in this locus and two transcript ... "Novel SH3 protein encoded by the AF3p21 gene is fused to the mixed lineage leukemia protein in a therapy-related leukemia with ... NCK-interacting protein with SH3 domain is a protein that in humans is encoded by the NCKIPSD gene. The protein encoded by this ... "Entrez Gene: NCKIPSD NCK interacting protein with SH3 domain". Satoh S, Tominaga T (October 2001). "mDia-interacting protein ...
MicroRNA Hepatocellular carcinoma Chronic lymphocytic leukemia Acute lymphoblastic leukemia Acute myeloid leukemia gastric MALT ... Its gene resembles a myeloid gene and it could be driven by the PU.1 and C/EBPα proteins which are myeloid transcription ... Higher expression levels of miRNA-223 are associated with extranodal marginal-zone lymphoma of mucosa-associated lymphoid ... acute lymphoblastic leukemia, acute myeloid leukemia, gastric MALT lymphoma, and recurrent ovarian cancer. Integrative analysis ...
So, it was named IL-9 based on its biological effects on both myeloid and lymphoid cells. The identification and cloning was ... Human IL-9 protein sequence contains 144 residues with a typical signal peptide of 18 amino acids. There is also the presence ... and sequences essential for its expression in human T-cell leukemia virus (HTLV)-I-transformed human T cells" (PDF). Blood. 77 ... proteins namely STAT1, STAT3 and STAT5 and thus connects this cytokine to various biological processes. The gene encoding this ...
January 2006). "Cbf beta-SMMHC induces distinct abnormal myeloid progenitors able to develop acute myeloid leukemia". Cancer ... CBFβ-SMMHC protein-protein interaction as a novel therapeutic avenue for leukemia with inv(16) and AI-10-49 as a specific ... Similarly, in adult hematopoiesis, CBF regulates the frequency and differentiation of HSCs, lymphoid and myeloid progenitors, ... and chronic myelomonocytic leukemia. In addition, RUNX1 mutations have also been reported in Acute myeloid leukemia (AML). The ...
Myeloid leukemias, myeloproliferative neoplasms, myeloid sarcomas, lymphoid leukemias, or non-Hodgkin lymphomas. Based on their ... These proteins have continuously active FGFR1-derived tyrosine kinase and thereby continuously stimulated the cell growth and ... These mutations occur in the early stages of myeloid and/or lymphoid cell lines and are the cause of or contribute to the ... Unlike many other myeloid neoplasms with eosinophil such as those caused by Platelet-derived growth factor receptor A or ...
... a lymphoid-specific G-protein-coupled receptor encoded on human chromosome 17q12-q21.2". Genomics. 23 (3): 643-650. doi:10.1006 ... "Increased chemokine receptor CCR7/EBI1 expression enhances the infiltration of lymphoid organs by adult T-cell leukemia cells ... is a chemoattractant with a specificity for macrophage progenitors among myeloid progenitor cells". Journal of Immunology. 161 ... CCR7 is a transmembrane protein with 7 transmembrane domains, which is coupled with heterotrimeric G proteins, which transduce ...
Myeloid-Lymphoid Leukemia Protein / genetics* * Phenotype* * Quantitative Trait Loci * Radiography * Sequence Deletion* ...
MLLT3 is involved with myeloid/lymphoid or mixed-lineage leukemia. PTPLAD2 is a protein tyrosine phosphatase. The exact ... KIAA1797 is a protein that in humans is encoded by the KIAA1797 gene. A specific single-nucleotide polymorphism rs7875153 in ... KIAA1797 is a protein-coding gene in Homo sapiens. Alternate names for the gene are FLJ20375, OTTHUMP00000069845, and ... The main isoform of the human protein is 1801 amino acids long, a total of 200,072 Da. Two distinct domains of unknown function ...
EVs were isolated from the serum of acute myeloid leukemia (AML), acute lymphoid leukemia (ALL), chronic lymphoid leukemia (CLL ... and EV surface protein profiles were analyzed by multiplex bead-based flow cytometry to identify tumor- or immune system- ... Special EV surface protein patterns in serum have the potential as noninvasive biomarker candidates to distinguish several ... EVs were isolated from the serum of acute myeloid leukemia (AML), acute lymphoid leukemia (ALL), chronic lymphoid leukemia (CLL ...
Protein description. 9 kDa , transcriptional regulatory factor; nuclear localisation. Gene name. KMT2A (myeloid/lymphoid or ... Panoramic view of common fusion genes in a large cohort of Chinese de novo acute myeloid leukemia patients.. 9. ... Protein description. 431 kDa; contains two DNA binding motifs (a AT hook, and Zinc fingers), a DNA methyl transferase motif, a ...
... novel mechanism that can enhance the function of a protein that is frequently impaired in patients with acute forms of leukemia ... help develop and ultimately test new treatment strategies for patients with either myeloid or lymphoid types of acute leukemia. ... Novel Mechanism Found That May Boost Impaired Function of Leukemia Protein Share * ... help develop and ultimately test new treatment strategies for patients with either myeloid or lymphoid types of acute leukemia ...
Solution structure of the first and second PHD domain from Myeloid/lymphoid or mixed-lineage leukemia protein 3 homolog. ... suggesting that this region may play an important functional role in protein-protein or protein-DNA interaction. HAT3.1 mRNA ... Overexpression of the Cyp33 protein in leukemia cells results in altered expression of HOX genes that are targets for ... Click on the protein counts, or double click on taxonomic names to display all proteins containing PHD domain in the selected ...
Solution structure of the first and second PHD domain from Myeloid/lymphoid or mixed-lineage leukemia protein 3 homolog. ... suggesting that this region may play an important functional role in protein-protein or protein-DNA interaction. HAT3.1 mRNA ... Overexpression of the Cyp33 protein in leukemia cells results in altered expression of HOX genes that are targets for ... Click on the protein counts, or double click on taxonomic names to display all proteins containing PHD domain in the selected ...
Blood cancers, or leukemias, affecting both myeloid and lymphoid cell lineages, are a further large area where MORE analysis ... but will not inhibit protein palmitoylation. In this respect our data clearly point out that RBC protein palmitoylation and not ... Thus, rapid analysis allows to establish the lineage of the leukemia (e.g. myeloid versus lymphoid), its stage of ... Acute myeloid/lymphatic leukemias. Request a detailed protocol Samples from patients diagnosed with ALL or AML based on ...
... approximately half of these DNMs disrupt gene function and the remainder result in altered protein function. We estimate that ... Myeloid-Lymphoid Leukemia Protein. , Nerve Tissue Proteins. , Parents. , Phenotype. , Prevalence. , Protein Phosphatase 2C. , ... CDC2 Protein Kinase. , Casein Kinase II. , Child. , Chromosomal Proteins, Non-Histone. , Cohort Studies. , DEAD-box RNA ... Homeodomain Proteins. , Humans. , Male. , Mi-2 Nucleosome Remodeling and Deacetylase Complex. , Middle Aged. , Mutation. , ...
MLL1 (Myeloid/lymphoid Or Mixed-Lineage Leukemia 1 (MLL1)) Andere Bezeichnung Myeloid/lymphoid or mixed-lineage leukemia 1 ( ... All of our reombinant proteins are expressed in E.coli. The standard are dissolved in PBS with 0.1 % proclin 300 and some other ... MLL1 (Myeloid/lymphoid Or Mixed-Lineage Leukemia 1 (MLL1)) Reaktivität Alle Reaktivitäten für MLL1 ELISA Kits * Dog 1 ... Myeloid/lymphoid Or Mixed-Lineage Leukemia 1 (MLL1) ELISA Kit MLL1 Reaktivität: Maus Colorimetric Competition ELISA 0.5-10 g/mL ...
Enl is a nuclear protein that is capable of activating transcription from synthetic reporter genes in both lymphoid and myeloid ... Chimeric RARalpha and acute myeloid leukemia 1 (AML1) proteins induce constitutive repression after the recruitment of ... Identification and characterization of leukemia stem cells in murine MLL-AF9 acute myeloid leukemia CANCER CELL Somervaille, T ... ENCODES A NUCLEAR-PROTEIN WITH TRANSCRIPTIONAL ACTIVATION POTENTIAL IN LYMPHOID AND MYELOID CELLS BLOOD Rubnitz, J. E., ...
Leukemia, Lymphoid; Ovarian Neoplasms; Leukemia, Myeloid; Hematologic Neoplasms; Solid tumours; Lymphoma, B-Cell, Marginal Zone ... Leukemia; Solid tumours; Myelodysplastic Syndromes; Lymphoma, Non-Hodgkin; Leukemia, Myeloid, Acute. Details ... Recombinant Proteins. GMP-grade Proteins Cell Therapy Targets Immune Checkpoints Cytokine Targets Other Proteins ViruStop: ... Solid tumours; Leukemia, Myelomonocytic, Chronic; Myelodysplastic Syndromes; Colorectal Neoplasms; Leukemia, Myeloid, Acute; ...
MLL, Proto-Oncogene Proteins Mixed Lineage Leukemia Protein Mixed-Lineage Leukemia Protein Myeloid Lymphoid Leukemia Protein ... MLL, Proto-Oncogene Proteins. Mixed Lineage Leukemia Protein. Mixed-Lineage Leukemia Protein. Myeloid Lymphoid Leukemia Protein ... Myeloid-Lymphoid Leukemia Protein - Preferred Concept UI. M0209080. Scope note. Myeloid-lymphoid leukemia protein is a ... Myeloid-Lymphoid Leukemia Protein Entry term(s). Acute Lymphoblastic Leukemia Protein 1 MLL Proto Oncogene Protein MLL Proto- ...
Myeloid-Lymphoid Leukemia Protein 100% * Vesicle-Associated Membrane Protein 2 88% * Clathrin 70% ...
Myeloid-Lymphoid Leukemia Protein 83% * Leukemia 77% * PHD Zinc Fingers 75% * Isomerization 73% ...
AP180 and clathrin assembly lymphoid myeloid leukemia protein (CALM) are clathrin accessory proteins that promote the formation ... AP180 and clathrin assembly lymphoid myeloid leukemia protein (CALM) are clathrin accessory proteins that promote the formation ... AP180 and clathrin assembly lymphoid myeloid leukemia protein (CALM) are clathrin accessory proteins that promote the formation ... AP180 and clathrin assembly lymphoid myeloid leukemia protein (CALM) are clathrin accessory proteins that promote the formation ...
Tumor protein p53; CDH1: Cadherin-1; MLL3: Myeloid/lymphoid or mixed-lineage leukemia protein 3; ESR1: Estrogen Receptor 1; ...
Non (protein)-coding RNAs are the most abundant transcriptional products of the coding genome, and comprise several different ... We discuss the value of lncRNAs as putative diagnostic, prognostic and therapeutic targets in myeloid leukemias and indicate ... Non (protein)-coding RNAs are the most abundant transcriptional products of the coding genome, and comprise several different ... Epigenetic regulation refers to the multiple chemical modifications of DNA or DNA-associated proteins that alter chromatin ...
The Bcr-Abl fusion protein kinase causes chronic myeloid leukemia and is targeted by the signal transduction inhibitor STI-571/ ... P230 forms of the BCR/ABL oncogene induce a similar chronic myeloid leukemia-like syndrome in mice but have different lymphoid ... Targeting the BCR-ABL tyrosine kinase in chronic myeloid leukemia [10].. *Characteristic of chronic myelogenous leukemia (CML) ... A mutation in the Icsbp1 gene causes susceptibility to infection and a chronic myeloid leukemia-like syndrome in BXH-2 mice. ...
MutS DNA Mismatch-Binding Protein. *MutS Homolog 2 Protein. *Myeloid-Lymphoid Leukemia Protein ... Immunoglobulin J Recombination Signal Sequence-Binding Protein*Immunoglobulin J Recombination Signal Sequence-Binding Protein ... The common oncogenomic program of NOTCH1 and NOTCH3 signaling in T-cell acute lymphoblastic leukemia. PLoS One. 2017; 12(10): ... Below are MeSH descriptors whose meaning is more general than "Immunoglobulin J Recombination Signal Sequence-Binding Protein". ...
These proteins being leukemogenic result in Chronic Myeloid leukemia (CML) and Acute lymphoid leukemia (ALL). Breakage in the ... The ratio of patients diagnosed with Chronic Myeloid Leukemia to Acute Lymphoid leukemia was 9.8:1. 9% of the patients had the ... results in the formation of a fusion hybrid gene also called Philadelphia chromosome encodes proteins with a constitutively ... These proteins being leukemogenic result in Chronic Myeloid leukemia (CML) and Acute lymphoid leukemia (ALL). Breakage in the ...
... or myeloid/lymphoid or mixed-lineage leukemia 4 genes causes upregulation of these oncogenes[95,96]. The upregulation of these ... The tumor suppressor protein P53 is a critical protein commonly mutated in cancer, that is involved in cell-cycle arrest at the ... Hepatitis C virus envelope proteins regulate CHOP via induction of the unfolded protein response. FASEB J. 2005;19:1510-1512. [ ... The tumor suppressor protein, p53, is targeted by many HCV proteins to prevent apoptosis, DNA-repair, and senescence. NS5A ...
... associated chronic eosinophilic leukemia is a form of blood cell cancer characterized by an elevated number of cells called ... Myeloid and lymphoid neoplasms associated with PDGFRA rearrangement. *Myeloid and lymphoid neoplasms with PDGFRA rearrangement ... Receptor proteins have specific sites into which certain other proteins, called ligands, fit like keys into locks. When the ... such as acute myeloid leukemia or B-cell or T-cell acute lymphoblastic leukemia or lymphoblastic lymphoma. ...
Its expression in specific subtypes of myeloid and lymphoid leukemias provides resistance to apoptosis and blocks further ... Computational analysis of SIL at the protein level revealed a 73% overall identity between the human and murine proteins. ... The distribution of MLL breakpoints for clinical subtypes (acute lymphoblastic leukemia, acute myeloid leukemia, pediatric and ... High expression of the ETS family transcription factor ERG is associated with poor clinical outcome in acute myeloid leukemia ( ...
... effective in patients with newly diagnosed or relapsed/refractory Philadelphia chromosome-positive acute lymphoblastic leukemia ... effective in patients with newly diagnosed or relapsed/refractory Philadelphia chromosome-positive acute lymphoblastic leukemia ... presentation includes data from 35 patients with Philadelphia chromosome-positive ALL or chronic myeloid leukemia in lymphoid ... that works by inhibiting proteins called tyrosine kinases on leukemia cells, in particular the abnormal BCR-ABL protein that ...
Myeloid/lymphoid or mixed lineage leukemia (trithorax homolog, Drosophila) PDB rendering based on 2j2s … Wikipedia ... Neural retina-specific leucine zipper protein is a protein that in humans is encoded by the NRL gene.[1][2][3] ... E2F (1, 2, 3, 4, 5) · FOX proteins (A1, A2, A3, C1, C2, D3, D4, E1, E3, F1, G1, H1, J1, J2, K1, K2, L2, M1, N1, N3, O1, O3, O4 ... MeSH NRL+protein,+human. This article incorporates text from the United States National Library of Medicine, which is in the ...
Myeloid-Lymphoid Leukemia Protein. *N-Myc Proto-Oncogene Protein. *Pre-B-Cell Leukemia Transcription Factor 1 ... "Proto-Oncogene Proteins c-mdm2" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH ( ... This graph shows the total number of publications written about "Proto-Oncogene Proteins c-mdm2" by people in this website by ... An E3 UBIQUITIN LIGASE that interacts with and inhibits TUMOR SUPPRESSOR PROTEIN P53. Its ability to ubiquitinate p53 is ...
... of beta ARK mRNA and kinase activity were found in peripheral blood leukocytes and in several myeloid and lymphoid leukemia ... we screened a number of G-protein-coupled receptor agonists for their ability to induce beta ARK translocation. In human ... of beta ARK mRNA and kinase activity were found in peripheral blood leukocytes and in several myeloid and lymphoid leukemia ... we screened a number of G-protein-coupled receptor agonists for their ability to induce beta ARK translocation. In human ...
... clathrin assembly lymphoid myeloid leukemia protein (CALM) was shown to have a function in KIT signaling in mouse HSCs (Rai et ... In another recent study, G-protein-coupled receptor-associated sorting proteins (GPRASP1) and GPRASP2, were found to be ... coating protein), Caveolin-1 (membrane protein associated with endocytosis), and GOPC (associated with Golgi). It has been ... "Clathrin assembly protein CALM plays a critical role in KIT signaling by regulating its cellular transport from early to late ...
  • Proto-Oncogene Proteins c-mdm2" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (umassmed.edu)
  • This graph shows the total number of publications written about "Proto-Oncogene Proteins c-mdm2" by people in this website by year, and whether "Proto-Oncogene Proteins c-mdm2" was a major or minor topic of these publications. (umassmed.edu)
  • Below are the most recent publications written about "Proto-Oncogene Proteins c-mdm2" by people in Profiles. (umassmed.edu)
  • A family of inhibitory proteins which bind to the REL PROTO-ONCOGENE PROTEINS and modulate their activity. (bvsalud.org)
  • Proto-Oncogene Proteins p21(ras)" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (uchicago.edu)
  • Below are the most recent publications written about "Proto-Oncogene Proteins p21(ras)" by people in Profiles. (uchicago.edu)
  • Acute leukemias induced by MLL chimeric oncoproteins are among the subset of cancers distinguished by a paradoxical dependence on GSK-3 kinase activity for sustained proliferation. (stanford.edu)
  • q 1.1)] results in the formation of a fusion hybrid gene also called Philadelphia chromosome encodes proteins with a constitutively activated tyrosine kinase activity [1,2]. (aku.edu)
  • Ponatinib is a targeted tyrosine kinase inhibitor (TKI) that works by inhibiting proteins called tyrosine kinases on leukemia cells, in particular the abnormal BCR-ABL protein that causes the disease. (mdanderson.org)
  • Very high levels of beta ARK mRNA and kinase activity were found in peripheral blood leukocytes and in several myeloid and lymphoid leukemia cell lines. (unich.it)
  • Protein kinase Cd and c-Abl kinase are required for transforming growth factor ß induction of endothelial-mesenchymal transition in vitro. (jefferson.edu)
  • EVs were isolated from the serum of acute myeloid leukemia (AML), acute lymphoid leukemia (ALL), chronic lymphoid leukemia (CLL) patients, and healthy volunteers. (nature.com)
  • These proteins being leukemogenic result in Chronic Myeloid leukemia (CML) and Acute lymphoid leukemia (ALL). (aku.edu)
  • The ratio of patients diagnosed with Chronic Myeloid Leukemia to Acute Lymphoid leukemia was 9.8:1. (aku.edu)
  • However, these circumstances do not account for the increased number of eosinophils in PDGFRA -associated chronic eosinophilic leukemia. (medlineplus.gov)
  • Another characteristic feature of PDGFRA -associated chronic eosinophilic leukemia is organ damage caused by the excess eosinophils. (medlineplus.gov)
  • People with PDGFRA -associated chronic eosinophilic leukemia can also have an enlarged spleen (splenomegaly) and elevated levels of certain chemicals called vitamin B12 and tryptase in the blood. (medlineplus.gov)
  • Some people with PDGFRA -associated chronic eosinophilic leukemia have an increased number of other types of white blood cells, such as neutrophils or mast cells. (medlineplus.gov)
  • Occasionally, people with PDGFRA -associated chronic eosinophilic leukemia develop other blood cell cancers, such as acute myeloid leukemia or B-cell or T-cell acute lymphoblastic leukemia or lymphoblastic lymphoma. (medlineplus.gov)
  • PDGFRA -associated chronic eosinophilic leukemia is often grouped with a related condition called hypereosinophilic syndrome. (medlineplus.gov)
  • PDGFRA -associated chronic eosinophilic leukemia is caused by mutations in the PDGFRA gene. (medlineplus.gov)
  • The most common genetic abnormality in PDGFRA -associated chronic eosinophilic leukemia results from a deletion of genetic material from chromosome 4 , which brings together part of the PDGFRA gene and part of the FIP1L1 gene, creating the FIP1L1-PDGFRA fusion gene. (medlineplus.gov)
  • When the FIP1L1-PDGFRA fusion gene mutation or point mutations in the PDGFRA gene occur in blood cell precursors, the growth of eosinophils (and occasionally other blood cells, such as neutrophils and mast cells) is poorly controlled, leading to PDGFRA -associated chronic eosinophilic leukemia. (medlineplus.gov)
  • The same five-year survival rate for patients diagnosed with acute myelogenous leukemia is around 14 percent, while an estimated 32 percent of patients with chronic myelogenous leukemia exceed this five-year survival period. (717698.com)
  • In laboratory experiments at Pennsylvania State University, researchers found that a component of Omega 3 known as Delta-12-J3 Prostaglandin or D12PGJ3 can selectively target the stem cells of chronic myelogenous leukemia or CML. (717698.com)
  • This enabled identification of TFs that can be uniquely associated to the tumor cells of chronic lymphocytic leukemia (CLL), diffuse large B-cell lymphoma (DLBCL), follicular lymphoma (FL), hairy cell leukemia (HCL), and mantle cell lymphoma (MCL). (lu.se)
  • Treatment protocols for chronic myelogenous leukemia are provided below for chronic phase, accelerated phase, and blast phase. (medscape.com)
  • See Chronic Leukemias: 4 Cancers to Differentiate , a Critical Images slideshow, to help detect chronic leukemias and determine the specific type present. (medscape.com)
  • Chronic lymphoid leukaemia and hairy cell leukaemia due to chronic exposure to benzene: Report of three cases. (cdc.gov)
  • Followup study on the mortality and the development of leukemia in 44 pancytopenic patients with chronic benzene exposure. (cdc.gov)
  • The GENE for myeloid-lymphoid leukemia protein is commonly disrupted in LEUKEMIA and combines with over 40 partner genes to form FUSION ONCOGENE PROTEINS. (bvsalud.org)
  • Chromosomal rearrangements of the human KMT2A/MLL gene are associated with de novo as well as therapy-induced infant, pediatric, and adult acute leukemias. (bvsalud.org)
  • This study provides a comprehensive analysis of the KMT2A recombinome in acute leukemia patients. (bvsalud.org)
  • The main isoform of the human protein is 1801 amino acids long, a total of 200,072 Da. (wikipedia.org)
  • The plant homeodomain (PHD) finger is a C4HC3 zinc-finger-like motif found in nuclear proteins thought to be involved in epigenetics and chromatin-mediated transcriptional regulation. (embl.de)
  • The function of this domain is not yet known but in analogy with the LIM domain it could be involved in protein-protein interaction and be important for the assembly or activity of multicomponent complexes involved in transcriptional activation or repression. (embl.de)
  • These are frequently activated by fusion to other transcriptional proteins resulting in chimeric transcription factors. (stanford.edu)
  • We are studying the effects and consequences of protein fusion on the transcriptional and transforming activities of these proteins using in vitro and animal models. (stanford.edu)
  • We demonstrate here that GSK-3 maintains the MLL leukemia stem cell transcriptional program by promoting the conditional association of CREB and its coactivators TORC and CBP with homedomain protein MEIS1, a critical component of the MLL-subordinate program, which in turn facilitates HOX-mediated transcription and transformation. (stanford.edu)
  • Non (protein)-coding RNAs are the most abundant transcriptional products of the coding genome, and comprise several different classes of molecules with unique lengths, conformations and targets. (frontiersin.org)
  • A ubiquitously expressed sequence-specific transcriptional repressor that is normally the target of signaling by NOTCH PROTEINS. (harvard.edu)
  • In order to get further insights into SF1 function and possible role in leukemogenesis, the aim of this project is to identify the splicing and transcriptional targets of SF1 in lymphoid cell line overexpressing this protein. (fapesp.br)
  • A broad category of receptor-like proteins that may play a role in transcriptional-regulation in the CELL NUCLEUS . (nih.gov)
  • Serine/arginine-rich protein-specific kinases (SRPKs) 1 and 2 phosphorylate and regulate serine/arginine-rich (SR) proteins that bind and regulate mRNA splicing, playing an important role in post-transcriptional regulation (1). (cellsignal.jp)
  • A cellular transcriptional coactivator that was originally identified by its requirement for the stable assembly IMMEDIATE-EARLY PROTEINS of the HERPES SIMPLEX VIRUS. (rush.edu)
  • KIAA1797 is a protein that in humans is encoded by the KIAA1797 gene. (wikipedia.org)
  • Neural retina-specific leucine zipper protein is a protein that in humans is encoded by the NRL gene . (en-academic.com)
  • SRPIN340 treatment of leukemia cells triggered early and late events of apoptosis, and reduced myeloid and lymphoid leukemia cell viability (3). (cellsignal.jp)
  • Recent study showed that iASPP could impact the proliferation and apoptosis of leukemia cells by interacting with FHL2 . (nature.com)
  • Bcl-2-deficient mice demonstrate fulminant lymphoid apoptosis, polycystic kidneys, and hypopigmented hair. (nature.com)
  • Leukemia and lymphoma are blood malignancies that affect people of all ages and result in approximately 23,000 deaths in the United States per year [ 1 ]. (nature.com)
  • Effective immune surveillance of patients with hematologic malignancies such as leukemia is mediated by cellular and noncellular arms of the innate and adaptive immune system. (nature.com)
  • Acute myeloid leukemia is a hematopoietic neoplasm of dismal prognosis that results from the accumulation of immature myeloid blasts in the bone marrow and the peripheral blood. (frontiersin.org)
  • We also identified a set of 83 genes that were highly expressed in leukemia blasts from patients without known molecular abnormalities who subsequently relapsed following therapy. (aacrjournals.org)
  • Leukemic blasts with prominent granules, often resembling multiple Auer rods, are a characteristic feature of Acute Myeloid Leukemia (AML). (labtestsguide.com)
  • The FIP1L1 gene provides instructions for a protein that plays a role in forming the genetic blueprints for making proteins (messenger RNA or mRNA). (medlineplus.gov)
  • Recently, somatic mutations within SF1 were reported in patients with myelodysplastic syndromes, de novo acute myeloid leukemia and myeloproliferative neoplasms. (fapesp.br)
  • Since agonist-induced beta ARK translocation is considered the first step involved in beta ARK-mediated homologous desensitization, we screened a number of G-protein-coupled receptor agonists for their ability to induce beta ARK translocation. (unich.it)
  • In the CYTOPLASM, I-kappa B proteins bind to the transcription factor NF-KAPPA B. Cell stimulation causes its dissociation and translocation of active NF-kappa B to the nucleus. (bvsalud.org)
  • Ten Eleven Translocation (TET) protein-catalyzed 5mC oxidation not only creates novel DNA modifications, such as 5hmC, but also initiates active or passive DNA demethylation. (researchgate.net)
  • Myeloid-lymphoid leukemia protein is a transcription factor that maintains high levels of HOMEOTIC GENE expression during development. (bvsalud.org)
  • The basic helix-loop-helix transcription factor SHARP1 is an oncogenic driver in MLL-AF6 acute myelogenous leukemia. (ox.ac.uk)
  • The CDK4-cyclinD complex normally phosphorylates the retinoblastoma protein (Rb protein), leading to release of the E2F transcription factor and cell cycle progression. (medscape.com)
  • Alternatively, the interactions could be intra-molecular and be important in maintaining the structural integrity of the protein. (embl.de)
  • In addition to these basic issues concerning leukemia pathogenesis, we are devising new diagnostic procedures for detecting and monitoring leukemia patients based on molecular genetic abnormalities in the malignant cells. (stanford.edu)
  • This mechanism also applies to hematopoietic cells transformed by other HOX genes, including CDX2, which is highly expressed in a majority of acute myeloid leukemias, thus providing a molecular approach based on GSK-3 inhibitory strategies to target HOX-associated transcription in a broad spectrum of leukemias. (stanford.edu)
  • Whether it is for protein electrophoresis or western blot, our pre-stained protein markers help you quickly determine the molecular weight of the target protein or evaluate the transfer efficiency. (acrobiosystems.com)
  • Clinical relevance of mutations and gene-expression changes in adult acute myeloid leukemia with normal cytogenetics: are we ready for a prognostically prioritized molecular classification? (nature.com)
  • Owing to the possibility of mismatching between antigens from another resource and antibodies used in this supplier's kits (e.g., antibody targets conformational epitope rather than linear epitope), some native or recombinant proteins from other manufacturers may not be recognized by this supplier's products. (antikoerper-online.de)
  • We discuss the value of lncRNAs as putative diagnostic, prognostic and therapeutic targets in myeloid leukemias and indicate novel directions in this exciting research field. (frontiersin.org)
  • In this thesis, we have addressed the importance of associating proteins in regulating FLT3 signaling as well as identified novel therapeutic targets to overcome FLT3-related resistance. (lu.se)
  • Panoramic view of common fusion genes in a large cohort of Chinese de novo acute myeloid leukemia patients. (atlasgeneticsoncology.org)
  • The protein, called AML1, plays a critical role in the development of the blood system and in the production of platelets and immune cells. (mskcc.org)
  • show that this approach can detect characteristic changes that affect blood cells as a result of malaria, spherocytosis, bacterial and viral infections, and leukemia. (elifesciences.org)
  • 3) We are defining the properties of cancer stem cells that initiate and sustain the unique disease features of acute leukemias through the use of various adoptive animal models. (stanford.edu)
  • Neural factors are a class of protein molecules with neurotrophic activity that can promote the survival and regeneration of nerve cells. (acrobiosystems.com)
  • Akin to the normal hematopoietic system, leukemias are sustained by a small number of leukemia stem-like cells (LSC), which can be distinct from the normal hematopoietic stem cells (HSC) but also exhibit functional characteristics of self-renewal and (abnormal or hindered) differentiation, and are often quiescent ( 2 - 4 ). (frontiersin.org)
  • It works by directing the T cells to target and bind with the CD19 protein on the surface of the leukemia cells. (mdanderson.org)
  • 2014). Given these findings, if we see colocalization between MYCT1 and any of our selected proteins, we can hypothesize its mechanistic role in hematopoietic cells according to the function of the proteins it colocalizes with. (ucla-mls.com)
  • Clathrin assembly protein CALM plays a critical role in KIT signaling by regulating its cellular transport from early to late endosomes in hematopoietic cells. (ucla-mls.com)
  • The HaeMa laboratory in Mannheim covers a broad range of hematological diagnostics for detecting diseases and disorders affecting the blood cells - from reactive changes to leukemias. (jenoptik.com)
  • Polymerase chain reaction -based qualitative and quantitative tests detect and measure the BCR-ABL1RNA transcripts in leukemia cells taken from blood or bone marrow samples. (717698.com)
  • In CML, the abnormal cells are a type of blood cell called myeloid cells. (717698.com)
  • CML is often suspected on the basis of a complete blood count, which shows increased granulocytes of all types, typically including mature myeloid cells. (717698.com)
  • More types of chemotherapeutics are required to kill all cancerous cells as Leukemia is known to spread very rapidly throughout the whole body. (717698.com)
  • To characterize gene expression signatures in acute lymphocytic leukemia (ALL) cells associated with known genotypic abnormalities in adult patients. (aacrjournals.org)
  • After more than four decades of intensive research, the cellular origins of acute lymphocytic leukemia (ALL) have been well defined, and several distinct genetic mechanisms that lead to malignant transformation of these cells have been identified ( 1 - 4 ). (aacrjournals.org)
  • In normal cells the BRCA1 protein is localized in the nucleus, whereas in the majority of breast cancer cell lines and in malignant pleural effusions from breast cancer patients, it is localized mainly in the cytoplasm. (jefferson.edu)
  • A clot is formed when fibrin, a fibrous protein, forms a mesh that entraps blood cells, primarily platelets and red blood cells, to stop bleeding and seal a wound when there is vascular injury. (labtestsguide.com)
  • Jude CD, Gaudet JJ, Speck NA, Ernst P. Leukemia and hematopoietic stem cells: balancing proliferation and quiescence. (nature.com)
  • FHL2 interacts with iASPP and impacts the biological functions of leukemia cells. (nature.com)
  • RUNX1-positive leukemia cells in preclinical models. (lu.se)
  • A combination of ponatinib and blinatumomab was found to be safe and highly effective in patients with newly diagnosed or relapsed/refractory Philadelphia chromosome-positive acute lymphoblastic leukemia (ALL), according to researchers at The University of Texas MD Anderson Cancer Center . (mdanderson.org)
  • For example, the TP53 gene, located on chromosome 17, encodes a 53-kd nuclear protein that functions as a cell cycle checkpoint. (medscape.com)
  • Genetic deletion in mice delays the development of leukemia and attenuated leukemia-initiating potential, while sparing normal hematopoiesis. (ox.ac.uk)
  • According to the study, investigators identified the methyltransferase enzyme that controls the activity of the normal AML1 protein - also called RUNX1 - demonstrating its ability to regulate the function of transcription factors, proteins that control cell fate by turning genes on or off. (mskcc.org)
  • The researchers found that the cellular pathways that regulate the activity of the normal AML1 protein through a process called arginine methylation cannot similarly regulate the activity of AML1-ETO, a protein associated with causing acute leukemia. (mskcc.org)
  • Our research focuses on developmental pathways that regulate hematopoietic cell growth and differentiation and are disrupted in the course of neoplastic transformation, particularly in leukemias and lymphomas. (stanford.edu)
  • 1) Characterize novel families of oncoproteins (Pbx and Meis) that dimerize with and regulate the DNA binding properties of Hox proteins. (stanford.edu)
  • We propose that both AP180 and CALM function as endocytic accessory proteins at synapses, but each may regulate distinct clathrin pathways. (elsevierpure.com)
  • PTPLAD2 is a protein tyrosine phosphatase. (wikipedia.org)
  • It contains an N-terminal RING FINGER DOMAIN and is a PROTEIN PHOSPHATASE 1 regulatory subunit. (jefferson.edu)
  • GPRASP proteins are critical negative regulators of hematopoietic stem cell transplantation. (ucla-mls.com)
  • EVs were characterized by transmission electron microscopy and fluorescence nanoparticle tracking analysis, and EV surface protein profiles were analyzed by multiplex bead-based flow cytometry to identify tumor- or immune system-related EVs of AML, ALL, CLL, and healthy samples. (nature.com)
  • Its ability to ubiquitinate p53 is regulated by TUMOR SUPPRESSOR PROTEIN P14ARF. (umassmed.edu)
  • [ 1 ] His prediction was subsequently supported by the cloning of the retinoblastoma tumor suppressor gene ( RB1 ) and by functional studies of the retinoblastoma protein, Rb. (medscape.com)
  • Like Rb protein, many of the proteins encoded by tumor suppressor genes act at specific points in the cell cycle. (medscape.com)
  • In addition, it is also important to exclude other, more specific AML categories (ie, AML with myelodysplasia-related changes, therapy-related myeloid neoplasm, AML with germline predisposition, myeloid proliferations related to Down syndrome) before classifying a condition as AML NOS. (medscape.com)
  • Many of these proteins are similar in structure to known NUCLEAR RECEPTORS but appear to lack a functional ligand-binding domain, while in other cases the specific ligands have yet to be identified. (nih.gov)
  • Immunoglobulin J Recombination Signal Sequence-Binding Protein" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (harvard.edu)
  • AP180 and clathrin assembly lymphoid myeloid leukemia protein (CALM) are clathrin accessory proteins that promote the formation of clathrin-coated vesicles. (elsevierpure.com)
  • Both proteins bind to membrane lipids through their epsin N-terminal homology domains and interact with clathrin and related protein components through their carboxyl-terminal peptide motifs. (elsevierpure.com)
  • 2016). Thus, we will assess MYCT1 colocalization with Syntaxin 6, and other vesicular trafficking candidates such as, EEA1, Rab 5A, APPL1, which are associated with endosomes, Clathrin Heavy Chain (coating protein), Caveolin-1 (membrane protein associated with endocytosis), and GOPC (associated with Golgi). (ucla-mls.com)
  • 2014). For example, clathrin assembly lymphoid myeloid leukemia protein (CALM) was shown to have a function in KIT signaling in mouse HSCs (Rai et al. (ucla-mls.com)
  • However, whether they have prognostic significance in acute myeloid leukemia (AML) is unknown. (nature.com)
  • They display considerable versatility in binding modes, even between members of the same class (e.g. some bind DNA, others protein), suggesting that Znf motifs are stable scaffolds that have evolved specialised functions. (embl.de)
  • Several reports suggest that it can function as a protein-protein interacton domain and it was recently demonstrated that the PHD finger of p300 can cooperate with the adjacent BROMO domain in nucleosome binding in vitro. (embl.de)
  • Explore our series of high-quality proteins covering comprehensive diagnostic indicators in order to facilitate the in vitro diagnostic research of neurological diseases. (acrobiosystems.com)
  • Our studies have demonstrated that several of the proteins encoded by cellular oncogenes function in fundamental aspects of gene regulation. (stanford.edu)
  • Emergence of LSC is dependent on individual or combined genetic mutations that broadly determine the cellular affiliation of the leukemia, and permit or impose ectopic self-renewal and a restricted differentiation potential into what constitutes the proliferative bulk of the leukemia ( 5 , 6 ). (frontiersin.org)
  • Cellular proteins encoded by the H-ras, K-ras and N-ras genes. (uchicago.edu)
  • Similarly, point mutations in the PDGFRA gene can result in a PDGFRA protein that is activated without ligand binding. (medlineplus.gov)
  • Acute myeloid leukemia (AML) is a highly heterogeneous blood disease which is characterized by different mutations and chromosomal rearrangements. (lu.se)
  • The FIP1L1-PDGFRA fusion gene (as well as other PDGFRA fusion genes) provides instructions for making a fusion protein that has the function of the normal PDGFRA protein. (medlineplus.gov)
  • However, the fusion protein does not require ligand binding to be activated. (medlineplus.gov)
  • Acute Myeloid Leukemia (AML) with MLL gene rearrangements demonstrate unique gene expression profiles driven by MLL-fusion proteins. (ox.ac.uk)
  • Histone modifications and chromatin-associated protein complexes are crucially involved in the control of gene expression, supervising cell fate decisions and differentiation. (researchgate.net)
  • c-Abl plays a role in normal HEMATOPOIESIS especially of the myeloid lineage. (jefferson.edu)
  • The PDGFRA gene provides instructions for making a receptor protein that is found in the cell membrane of certain cell types. (medlineplus.gov)
  • We are investigating how Pbx and Meis proteins contribute to the specificity of Hox function in development and how disruption of their activities leads to neoplasia. (stanford.edu)